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How Does A Muscle Tear Repair Itself

Written By Monday, February 21, 2022 Add Comment Edit

J Exp Orthop. 2016 Dec; 3: 15.

Muscle injuries and strategies for improving their repair

Thomas Laumonier

Department of Orthopaedic Surgery, Geneva University Hospitals & Faculty of Medicine, 4, Rue Gabrielle Perret-Gentil, 1211 Geneva xiv, Switzerland

Jacques Menetrey

Department of Orthopaedic Surgery, Geneva Academy Hospitals & Faculty of Medicine, iv, Rue Gabrielle Perret-Gentil, 1211 Geneva 14, Switzerland

Received 2016 Mar 15; Accustomed 2016 Jul 15.

Abstract

Satellite cells are tissue resident muscle stalk cells required for postnatal skeletal muscle growth and repair through replacement of damaged myofibers. Muscle regeneration is coordinated through different mechanisms, which imply cell-cell and cell-matrix interactions as well every bit extracellular secreted factors. Cellular dynamics during musculus regeneration are highly complex. Allowed, fibrotic, vascular and myogenic cells announced with distinct temporal and spatial kinetics subsequently muscle injury. Three main phases accept been identified in the process of muscle regeneration; a destruction phase with the initial inflammatory response, a regeneration phase with activation and proliferation of satellite cells and a remodeling phase with maturation of the regenerated myofibers. Whereas relatively minor muscle injuries, such every bit strains, heal spontaneously, severe muscle injuries form fibrotic tissue that impairs muscle role and lead to musculus contracture and chronic pain. Electric current therapeutic approaches accept limited effectiveness and optimal strategies for such lesions are not known nonetheless. Diverse strategies, including growth factors injections, transplantation of muscle stem cells in combination or not with biological scaffolds, anti-fibrotic therapies and mechanical stimulation, may become therapeutic alternatives to better functional muscle recovery.

Keywords: Skeletal musculus, Injury, Regeneration, Stalk cell, Fibrosis, Scaffolds, Growth factors

Introduction

Human being skeletal muscle is nigh xl % of the torso mass and is formed by parcel of contractile multinucleated muscle fibers, resulting from the fusion of myoblasts. Satellite cells (SC) are skeletal muscle stalk cell located between the plasma membrane of myofibers and the basal lamina. Their regenerative capabilities are essential to repair skeletal muscle afterward injury (Hurme and Kalimo 1992; Lipton and Schultz 1979) (Sambasivan et al. 2011; Dumont et al. 2015a). In adult muscles, SC are constitute in a quiescent state and correspond, depending on species, age, muscle location, and musculus type, around 5 to ten % of skeletal musculus cells (Rocheteau et al. 2015). Afterwards injury, SC go activated, proliferate and give rise to myogenic forerunner cells, known as myoblasts. After entering the differentiation process, myoblasts form new myotubes or fuse with damaged myofibers, ultimately mature in functional myofibers.

Skeletal muscle injuries can stem from a variety of events, including directly trauma such every bit muscle lacerations and contusions, indirect insults such as strains and also from degenerative diseases such every bit muscular dystrophies (Huard et al. 2002; Kasemkijwattana et al. 2000; Kasemkijwattana et al. 1998; Menetrey et al. 2000; Menetrey et al. 1999; Crisco et al. 1994; Garrett et al. 1984; Lehto and Jarvinen 1991; Jarvinen et al. 2005; Cossu and Sampaolesi 2007). Skeletal muscle can regenerate completely and spontaneously in response to minor injuries, such equally strain. In contrast, after astringent injuries, muscle healing is incomplete, oftentimes resulting in the germination of fibrotic tissue that impairs musculus function. Although researchers take extensively investigated various approaches to improve muscle healing, there is nonetheless no gilt standard treatment.

This concise review provides a sight about the diverse phases of muscle repair and regeneration, namely degeneration, inflammation, regeneration, remodeling and maturation. Nosotros also give an overview of inquiry efforts that have focused on the apply of stalk cell therapy, growth factors and/or biological scaffolds to meliorate musculus regeneration and repair. We likewise address the therapeutic potential of mechanical stimulation and of anti-fibrotic therapy to enhance muscle regeneration and repair.

Review

Musculus healing process

Skeletal musculus has a robust innate adequacy for repair after injury through the presence of adult muscle stem cells known equally satellite cells (SC). The disruption of muscle tissue homeostasis, caused past injury, generates sequential involvement of various players around three main phases (Fig.1).

  • (1, 2) Degeneration/inflammation phase: characterized by rupture and necrosis of the myofibers, formation of a hematoma and an important inflammatory reaction.

  • (3) Regeneration phase: phagocytosis of damaged tissue, followed by myofibers regeneration, leading to satellite jail cell activation.

  • (four, 5) Remodeling stage: maturation of regenerated myofibers with recovery of muscle functional chapters (iv) and also fibrosis and scar tissue germination (5).

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Sequential bicycle of muscle healing phases after laceration. Histological images adapted from Menetrey et al, Am J Sports Med 1999. (sp: superficial portion, de: deepest part)

Musculus degeneration and inflammation

Active muscle degeneration and inflammation occur within the first few days after injury. The initial outcome is necrosis of the musculus fibers, which is triggered by disruption of local homeostasis and especially past unregulated influx of calcium through sarcolemma lesions (Tidball 2011). Excess in cytoplasmic calcium causes proteases and hydrolases activation that contribute to musculus damage and likewise causes activation of enzymes that drive the production of mitogenic substances for muscle and immune cells (Tidball 2005). After muscle degeneration, neutrophils are the kickoff inflammatory cells infiltrating the lesion. A large number of pro-inflammatory molecules such every bit cytokines (TNF-α, IL-half-dozen), chemokine (CCL17, CCL2) and growth factors (FGF, HGF, IGF-I, VEGF; TGF-β1) are secreted past neutrophils in order to create a chemoattractive microenvironment for other inflammatory cells such as monocytes and macrophages (Tidball 1995; Toumi and Best 2003). Two types of macrophages are identified during muscle regeneration (McLennan 1996), which appear sequentially during muscle repair (Arnold et al. 2007). M1 macrophages, defined equally pro-inflammatory macrophages, act during the first few days after injury,. contribute to cell lysis, removal of cellular debris and stimulate myoblast proliferation. Conversely, M2 macrophages, divers equally anti-inflammatory macrophages, human action 2 to 4 days after injury, attenuate the inflammatory response and favor muscle repair by promoting myotubes formation (Tidball and Wehling-Henricks 2007; Chazaud 2014; Chazaud et al. 2003). Macrophages, infiltrating injured muscle, are key players of the healing procedure (Zhao et al. 2016), able to participate in the muscle regeneration process or to favor fibrosis (Munoz-Canoves and Serrano 2015; Lemos et al. 2015).

Musculus regeneration, remodeling and maturation

Muscle regeneration usually starts during the showtime iv–5 days after injury, peaks at ii weeks, and and so gradually diminishes 3 to iv weeks later on injury. It'southward a multiple steps process including activation/proliferation of SC, repair and maturation of damaged muscle fibers and connective tissue formation. A fine balance between these mechanisms is essential for a full recovery of the contractile muscle office.

Muscle fibers are post-mitotic cells, which do not accept the chapters to divide. Following an injury, damaged musculus fibers can't exist repaired without the presence of developed muscle stalk cells, the satellite cells (SC) (Relaix and Zammit 2012; Sambasivan et al. 2011). Following activation, SC proliferate and generate a population of myoblasts that can either differentiate to repair damaged fibers or, for a small proportion, self-renew to maintain the SC pool for possible future demands of muscle regeneration (Collins 2006; Dhawan and Rando 2005). SC wheel progression and cell fate determination are control past circuitous regulatory mechanisms in which, intrinsic and extrinsic factors are involved (Dumont et al. 2015a; Dumont et al. 2015b).

Connective tissue/fibrosis

Connective tissue remodeling is an important step of the regenerative muscle process. Rapidly after musculus injury, a gap is formed between damaged muscle fibers and filled with a hematoma. Muscle injuries tin can be clinically classified depending of the nature of the hematoma (size, location). Late emptying of the hematoma is known to delay skeletal muscle regeneration, to improve fibrosis and to reduce biomechanical properties of the healing muscle (Beiner et al. 1999). In rare complication, major muscle injuries may atomic number 82 to the evolution of myositis ossificans that will impair musculus regeneration and repair (Beiner and Jokl 2002) (Walczak et al. 2015).

The presence of fibrin and fibronectin at the injury site, initiate the formation of an extracellular matrix that is rapidly invaded past fibroblasts (Darby et al. 2016; Desmouliere and Gabbiani 1995). Fibrogenic cytokines such as transforming growth factor β1 (TGF-β1) participate to excessive fibroblasts/myofibroblasts proliferation and to an increase in type I/III collagens, laminin and fibronectin production (Lehto et al. 1985). In its initial phase, the fibrotic response is benign, stabilizing the tissue and acting every bit a scaffold for myofibers regeneration. Nevertheless, an excessive collagen synthesis post injury, often effect in an increase of scar tissue size over time that can prevent normal muscle part (Isle of man et al. 2011). Many growth factors are involved in the development of fibrosis, such equally Connective Tissue Growth Factor (CTGF), Platelet-Derived Growth Gene (PDGF) or myostatin. TGF-β1, past stimulating fibroblasts/myofibroblasts to produce extracellular proteins such as fibronectin and type I/III collagen, has been identified as the primal element in this process (Isle of man et al. 2011),. Although fibroblasts are the major collagen-producing cells in skeletal muscle, TGF-β1 take also an issue directly on myoblasts causing their conversion to myofibroblasts. Thus myoblasts initially acting to repair damaged myofibers, will produce meaning level of collagen and will contribute to muscle fibrosis (Li and Huard 2002).

R evascularization

The restoration of the blood supply in the injured skeletal musculus is one of the first signs of musculus regeneration and is essential to its success. Without revascularization, muscle regeneration is incomplete and a pregnant fibrosis occurs (Best et al. 2012; Ota et al. 2011). Later muscle trauma, blood vessels rupture induces tissue hypoxia at the injury site (Jarvinen et al. 2005). New capillaries formation quickly after injury is therefore necessary (Scholz et al. 2003) for a functional muscle recovery. Secretion of angiogenic factors such as vascular endothelial growth gene (VEGF) at the lesion site is important and several studies have shown that VEGF, by favoring angiogenesis, improve skeletal musculus repair (Deasy et al. 2009; Frey et al. 2012).

Innervation

Muscle repair is complete when injured myofibers are fully regenerated and become innervated. The synaptic contact between a motor neuron and its target muscle fiber, often take identify at a specific site in the central region of myofibers, the neuromuscular junction (NMJ) (Wu et al. 2010). NMJ are essential for maturation and functional activity of regenerating muscles. Inside 2–3 weeks after muscle damage, the presence of newly formed NMJ is observed in regenerative musculus (Rantanen et al. 1995; Vaittinen et al. 2001).

Strategies to improve muscle regeneration and repair

Growth factors

Growth factors play a variety of roles in the different stages of muscle regeneration (Grounds 1999; Menetrey et al. 2000). These biologically active molecules, synthetized by the injured tissue or by other prison cell types present at the inflammatory site, are release in the extracellular space and modulate the regenerative response (Table1). Although hepatocyte growth factor (HGF), fibroblast growth factor (FGF) and platelet-derived growth cistron (PDGF) are of interest because of their capacity to stimulate satellite cells (Sheehan et al. 2000; Allen and Boxhorn 1989; Yablonka-Reuveni et al. 1990), insulin like growth cistron-1 (IGF-I) appears to be of detail importance for the muscle regeneration process. IGF-I stimulates myoblasts proliferation and differentiation (Engert et al. 1996) and is implicated in the regulation of musculus growth (Schiaffino and Mammucari 2011). In a mouse model, direct injections of human recombinant IGF-I at two, v, and seven days after injury enhanced muscle healing in lacerated, contused, and strain-injured muscles (Menetrey et al. 2000; Kasemkijwattana et al. 2000). Nevertheless, the efficacy of direct injection of recombinant proteins is limited by the high concentration of the cistron typically required to elicit a measurable effect. This is mainly due to the bloodstream's rapid clearance of these molecules and their relatively short biological one-half-lives. Gene therapy may be an effective method by which to evangelize high, maintainable concentrations of growth factor to injured musculus (Barton-Davis et al. 1998; Barton et al. 2002; Musaro et al. 2001). Although IGF-I improved muscle healing, histology of the injected muscle revealed fibrosis inside the lacerated site, despite high level of IGF-I production (Lee et al. 2000). Another growth factor, VEGF, by favoring angiogenesis, is known to enhance skeletal muscle repair (Deasy et al. 2009; Frey et al. 2012; Messina et al. 2007). By targeting simultaneously angiogenesis and myogenesis, it was shown that combined delivery of VEGF and IGF-I enhance muscle regenerative process (Borselli et al. 2010). In this direction, the use of platelet-rich plasma (PRP) is considered as a possible alternative approach based on the power of autologous growth factors to better skeletal muscle regeneration (Hamid et al. 2014; Hammond et al. 2009). Considered as safe products, autologous PRP injections are increasingly used in patients with sports-related injuries (Engebretsen et al. 2010). Yet, a contempo randomized clinical trial show no meaning positive effects of PRP injections, equally compared with placebo injections, in patients with musculus injuries, up to one twelvemonth afterwards injections (Reurink et al. 2014; Reurink et al. 2015). Customization of PRP preparation, as recently demonstrated by the use of TGF-β1 neutralizing antibodies, is a promising alternative to promote muscle regeneration while significantly reducing fibrosis (Li et al. 2016).

Table 1

The role of growth factors in skeletal muscle regeneration

Growth factors Physiological effects, potential benefits Shortcomings Commentary
IGF-1 - Essential for muscle growth during development and regeneration.
- Promote myoblast proliferation and differentiation in vitro (Huard et al. 2002)
- Hypertrophic issue of IGF-1 (Barton-Davis et al. 1999)
- Serial injections of IGF-ane better muscle healing in vivo (Menetrey et al. 2000).
- Being of a muscle specific isoform of IGF-1 (mIGF-1) (Musaro et al. 1999; Musaro et al. 2004)		 - Chemotactic for fibroblasts, increase collagen production, enhance fibrosis evolution - IGF-ane play a fundamental office in the enhancement of muscle regeneration-
- Anti-inflammatory actions of IGF-1 (Mourkioti and Rosenthal 2005; Tidball and Welc 2015)
HGF - Promote myoblast proliferation and inhibit myoblast differentiation (Anderson 2016; Yin et al. 2013)
- Important role for satellite cell activation. Balance between the activation of satellite cells and their return to quiescence. (Chazaud 2010)
- Recently, it was shown that a 2nd set of HGF production is crucial for inflammation resolution after injury (Proto et al. 2015)		 - Injection of HGF into injured muscle increased myoblast numbers merely blocked the regeneration process (Miller et al. 2000) - HGF is important during the early phase of muscle regeneration, activate satellite cells
VEGF - Important signaling protein that favor angiogenesis.
- Promote myoblast migration, proliferation and survival. (Arsic et al. 2004)
- VEGF administration improves muscle regeneration. (Messina et al. 2007; Deasy et al. 2009)		 - Non regulated VEGF expression promote aberrant angiogenesis and fibrosis in skeletal musculus (Karvinen et al. 2011) - Importance of the proximity between satellite cells and the microvasculature during muscle regeneration, role of VEGF
FGF - Large family of mitogen involved in cell growth and survival
- FGF-6 has a muscle specific expression, stimulates satellite cell proliferation and promotes myogenic concluding differentiation (Floss et al. 1997)
- FGF-two promote satellite prison cell proliferation and inhibit myogenic differentiation (Menetrey et al. 2000; Kastner et al. 2000)		 - Stimulate fibroblast proliferation, - FGF signaling plays a central role in musculus repair, blocking FGF signaling filibuster muscle regeneration (Saera-Vila et al. 2016).
TGF-β1 - Key regulator of the residuum betwixt muscle fibrosis and muscle regeneration
- Inhibits satellite cell proliferation and differentiation in vitro		 - Excessive TGFβ1-induced deposition of ECM at the site of injury, fibrosis (Garg et al. 2015). - Anti fibrotic therapy by blocking overexpression of TGF-β1 amend muscle regeneration. (Burks et al. 2011; Hwang et al. 2016)
PDGF-BB - PDGF isoforms can regulate myoblast proliferation and differentiation in vitro (Yablonka-Reuveni et al. 1990)
- PDGF-BB stimulates satellite cell proliferation and inhibit their differentiation (Charge and Rudnicki 2004)		 - Potent mitogen for fibroblasts - Release from injured vessels and platelets, PDGF stimulates early on skeletal muscle regeneration

Stalk cells

Transplantation of satellite prison cell-derived myoblasts has long been explored every bit a promising approach for handling of skeletal musculus disorders. After an initial demonstration that normal myoblasts can restore dystrophin expression in mdx mice (Partridge et al. 1989), clinical trials, in which allogeneic normal human myoblasts were injected intramuscularly several times in dystrophic immature boys muscles, have not been successful (Police force et al. 1990; Mendell et al. 1995). Even recently, despite clear improvement in methodologies that heighten the success of myoblast transplantation in Duchenne patients (Skuk et al. 2007), outcomes of clinical trials are still disappointing. These experiments have raised concerns about the limited migratory and proliferative capacities of man myoblasts, every bit well as their express life span in vivo. It led to the investigations of other muscle stem cells sources that could overcome these limitations and outperform the success of musculus cell transplantation. Among all these non-satellite myogenic stem cells, human mesoangioblasts, human myogenic-endothelial cells and human musculus–derived CD133+ take shown myogenic potentials in vitro and in vivo (Sampaolesi et al. 2006; Zheng et al. 2007; Meng et al. 2014). The use of such myogenic progenitors cells for improving musculus healing may get an interesting therapeutic culling (Tedesco and Cossu 2012; Tedesco et al. 2010; Chen et al. 2012). A first phase I/IIa clinical trial has recently demonstrated that intra arterial injections of human mesoangioblasts are prophylactic merely display merely very limited clinical efficacy in Duchenne patients (Cossu et al. 2015).

Scaffolds

Myogenic precursor cell survival and migration is greatly increased past using appropriate scaffold composition and growth factor commitment (Hill et al. 2006) (Boldrin et al. 2007). Controlling the microenvironment of injected myogenic cells using biological scaffolds enhance muscle regeneration (Borselli et al. 2011). Ideally, using an appropriate extracellular matrix (ECM) composition and stiffness, scaffolds should all-time replicate the in vivo milieu and mechanical microenvironment (Gilbert et al. 2010) (Engler et al. 2006). A combination of stalk cells, biomaterial-based scaffolds and growth factors may provide a therapeutic option to improve regeneration of injured skeletal muscles (Jeon and Elisseeff 2016).

Anti-fibrotic therapy

TGF-β1 is expressed at high levels and plays an of import function in the fibrotic pour that occurs later the onset of muscle injury (Bernasconi et al. 1995; Li et al. 2004). Therefore, neutralization of TGF-β1 expression in injured skeletal muscle should inhibit the formation of scar tissue. Indeed, the use of anti-fibrotic agents (ie decorin, relaxin, antibody against TGF-β1…) that inactivate TGF-β1 signaling pathways reduces musculus fibrosis and, consequently, better muscle healing, leading to a near complete recovery of lacerated musculus (Fukushima et al. 2001; Li et al. 2007). Losartan, an angiotensin Ii receptor antagonist, neutralize the effect of TGF-β1 and reduce fibrosis, making it the treatment of choice, since it already has FDA approval to exist used clinically (Bedair et al. 2008; Park et al. 2012; Terada et al. 2013). Suramin, also approved by the FDA, blocks TGF-β1 pathway and reduces muscle fibrosis in experimental model (Chan et al. 2003; Taniguti et al. 2011).

Mechanical stimulation

Mechanical stimulation may offer a simple and constructive arroyo to enhance skeletal musculus regeneration. Stretch activation, mechanical conditioning but also massage therapy or physical manipulation of injured skeletal muscles have shown multiple benefit furnishings on muscle biological science and office in vitro and in vivo (Tatsumi et al. 2001);(Best et al. 2012) (Crane et al. 2012; Kumar et al. 2002; Gilbert et al. 2010; Powell et al. 2002). Recently, Cezar and colleagues demonstrates that mechanical forces are equally important biological regulators equally chemicals and genes, and underlines the immense potential of developing mechano-therapies to treat muscle damage (Cezar et al. 2016). A recent report too demonstrated that a treatment based on ultrasound-guided intra-tissue percutaneous electrolysis (EPI technique) enhances the treatment of muscle injuries (Abat et al. 2015). Altogether, these results suggest that mechanical stimulation should be considered as a possible therapy to improve muscle regeneration and repair.

Conclusions

Skeletal muscle injuries are very frequently present in sports medicine and pose challenging bug in traumatology. Despite their clinical importance, the optimal rehabilitation strategies for treating these injuries are not well defined. After a trauma, skeletal muscles have the capacity to regenerate and repair in a circuitous and well-coordinated response. This process required the presence of various cell populations, up and downward-regulation of various factor expressions and participation of multiples growth factors. Strategies based on the combination of stem cells, growth factors and biological scaffolds take already shown promising results in brute models. A meliorate understanding of the cellular and molecular pathways as well as a better definition of the interactions (cell-cell and jail cell-matrix) that are essential for effective musculus regeneration, should contribute to the development of new therapies in humans. In this direction, a contempo paper from Sadtler et al demonstrated that specific biological scaffold implanted in injured mice muscles trigger a pro-regenerative immune response that stimulate skeletal muscle repair (Sadtler et al. 2016).

Abbreviation

CTGF, connective tissue growth factor; FGF, fibroblast growth factor; HGF, hepatocyte growth factor; IGF-I, insulin like growth factor-I; NMJ, neuromuscular junction; PDGF, platelet derived growth factor; PRP, platelet rich plasma; SC, satellite cells; TGF-β1, transforming growth factor β1; VEGF, vascular endothelial growth gene

Footnotes

Competing interests

The authors declare that they take no competing interests.

Authors' contributions

TL and JM participated equally in drafting the manuscript. Both authors read and canonical the final manuscript.

References

  • Abat F, Valles SL, Gelber PE, Polidori F, Jorda A, Garcia-Herreros S, Monllau JC, Sanchez-Ibanez JM. An experimental study of muscular injury repair in a mouse model of notexin-induced lesion with EPI(R) technique. BMC Sports Sci Med Rehabil. 2015;7:seven. doi: x.1186/s13102-015-0002-0. [PMC gratuitous article] [PubMed] [CrossRef] [Google Scholar]
  • Allen RE, Boxhorn LK. Regulation of skeletal muscle satellite cell proliferation and differentiation past transforming growth factor-beta, insulin-like growth factor I, and fibroblast growth cistron. J Jail cell Physiol. 1989;138(2):311–315. doi: x.1002/jcp.1041380213. [PubMed] [CrossRef] [Google Scholar]
  • Anderson JE. Hepatocyte growth gene and satellite cell activation. Adv Exp Med Biol. 2016;900:1–25. doi: x.1007/978-3-319-27511-6_1. [PubMed] [CrossRef] [Google Scholar]
  • Arnold L, Henry A, Poron F, Baba-Amer Y, van Rooijen N, Plonquet A, Gherardi RK, Chazaud B. Inflammatory monocytes recruited after skeletal musculus injury switch into antiinflammatory macrophages to support myogenesis. J Exp Med. 2007;204(5):1057–1069. doi: 10.1084/jem.20070075. [PMC costless article] [PubMed] [CrossRef] [Google Scholar]
  • Arsic North, Zacchigna S, Zentilin L, Ramirez-Correa G, Pattarini L, Salvi A, Sinagra One thousand, Giacca One thousand. Vascular endothelial growth gene stimulates skeletal musculus regeneration in vivo. Mol Ther. 2004;10(five):844–854. doi: 10.1016/j.ymthe.2004.08.007. [PubMed] [CrossRef] [Google Scholar]
  • Barton ER, Morris L, Musaro A, Rosenthal N, Sweeney HL. Muscle-specific expression of insulin-like growth factor I counters musculus refuse in mdx mice. J Prison cell Biol. 2002;157(1):137–148. doi: ten.1083/jcb.200108071. [PMC free article] [PubMed] [CrossRef] [Google Scholar]
  • Barton-Davis ER, Shoturma DI, Musaro A, Rosenthal N, Sweeney HL. Viral mediated expression of insulin-like growth factor I blocks the crumbling-related loss of skeletal muscle function. Proc Natl Acad Sci U S A. 1998;95(26):15603–15607. doi: 10.1073/pnas.95.26.15603. [PMC free article] [PubMed] [CrossRef] [Google Scholar]
  • Barton-Davis ER, Shoturma DI, Sweeney HL. Contribution of satellite cells to IGF-I induced hypertrophy of skeletal muscle. Acta Physiol Scand. 1999;167(four):301–305. doi: 10.1046/j.1365-201x.1999.00618.x. [PubMed] [CrossRef] [Google Scholar]
  • Bedair HS, Karthikeyan T, Quintero A, Li Y, Huard J. Angiotensin II receptor blockade administered after injury improves muscle regeneration and decreases fibrosis in normal skeletal musculus. Am J Sports Med. 2008;36(viii):1548–1554. doi: 10.1177/0363546508315470. [PubMed] [CrossRef] [Google Scholar]
  • Beiner JM, Jokl P (2002) Muscle contusion injury and myositis ossificans traumatica. Clin Orthop Relat Res (403 Suppl):S110-119 [PubMed]
  • Beiner JM, Jokl P, Cholewicki J, Panjabi MM. The effect of anabolic steroids and corticosteroids on healing of musculus contusion injury. Am J Sports Med. 1999;27(1):2–9. [PubMed] [Google Scholar]
  • Bernasconi P, Torchiana Due east, Confalonieri P, Brugnoni R, Barresi R, Mora M, Cornelio F, Morandi L, Mantegazza R. Expression of transforming growth factor-beta 1 in dystrophic patient muscles correlates with fibrosis. Pathogenetic office of a fibrogenic cytokine. J Clin Invest. 1995;96(2):1137–1144. doi: 10.1172/JCI118101. [PMC gratis article] [PubMed] [CrossRef] [Google Scholar]
  • Best TM, Gharaibeh B, Huard J. Stem cells, angiogenesis and musculus healing: a potential part in massage therapies? Br J Sports Med. 2012 [PubMed] [Google Scholar]
  • Boldrin L, Elvassore N, Malerba A, Flaibani M, Cimetta E, Piccoli M, Baroni Medico, Gazzola MV, Messina C, Gamba P, Vitiello L, de Coppi P. Satellite cells delivered past micro-patterned scaffolds: a new strategy for cell transplantation in muscle diseases. Tissue Eng. 2007;13(2):253–262. doi: 10.1089/10.2006.0093. [PubMed] [CrossRef] [Google Scholar]
  • Borselli C, Storrie H, Benesch-Lee F, Shvartsman D, Cezar C, Lichtman JW, Vandenburgh HH, Mooney DJ. Functional muscle regeneration with combined delivery of angiogenesis and myogenesis factors. Proc Natl Acad Sci U S A. 2010;107(8):3287–3292. doi: 10.1073/pnas.0903875106. [PMC complimentary commodity] [PubMed] [CrossRef] [Google Scholar]
  • Borselli C, Cezar CA, Shvartsman D, Vandenburgh HH, Mooney DJ. The role of multifunctional delivery scaffold in the ability of cultured myoblasts to promote muscle regeneration. Biomaterials. 2011;32(34):8905–8914. doi: 10.1016/j.biomaterials.2011.08.019. [PMC free article] [PubMed] [CrossRef] [Google Scholar]
  • Burks TN, Andres-Mateos E, Marx R, Mejias R, Van Erp C, Simmers JL, Walston JD, Ward CW, Cohn RD. Losartan restores skeletal muscle remodeling and protects against disuse cloudburst in sarcopenia. Sci Transl Med. 2011;three(82):82ra37. doi: 10.1126/scitranslmed.3002227. [PMC free article] [PubMed] [CrossRef] [Google Scholar]
  • Cezar CA, Roche ET, Vandenburgh HH, Duda GN, Walsh CJ, Mooney DJ. Biologic-gratuitous mechanically induced muscle regeneration. Proc Natl Acad Sci U S A. 2016;113(half-dozen):1534–1539. doi: 10.1073/pnas.1517517113. [PMC complimentary article] [PubMed] [CrossRef] [Google Scholar]
  • Chan YS, Li Y, Foster W, Horaguchi T, Somogyi M, Fu FH, Huard J. Antifibrotic effects of suramin in injured skeletal muscle after laceration. J Appl Physiol. 2003;95(2):771–780. doi: 10.1152/japplphysiol.00915.2002. [PubMed] [CrossRef] [Google Scholar]
  • Charge SB, Rudnicki MA. Cellular and molecular regulation of musculus regeneration. Physiol Rev. 2004;84(1):209–238. doi: ten.1152/physrev.00019.2003. [PubMed] [CrossRef] [Google Scholar]
  • Chazaud B. Dual outcome of HGF on satellite/myogenic jail cell quiescence. Focus on "High concentrations of HGF inhibit skeletal muscle satellite cell proliferation in vitro by inducing expression of myostatin: a possible machinery for reestablishing satellite cell quiescence in vivo". Am J Physiol Cell Physiol. 2010;298(three):C448–C449. doi: 10.1152/ajpcell.00561.2009. [PubMed] [CrossRef] [Google Scholar]
  • Chazaud B. Macrophages: supportive cells for tissue repair and regeneration. Immunobiology. 2014;219(three):172–178. doi: 10.1016/j.imbio.2013.09.001. [PubMed] [CrossRef] [Google Scholar]
  • Chazaud B, Sonnet C, Lafuste P, Bassez G, Rimaniol Air-conditioning, Poron F, Authier FJ, Dreyfus PA, Gherardi RK. Satellite cells concenter monocytes and apply macrophages as a back up to escape apoptosis and enhance muscle growth. J Cell Biol. 2003;163(v):1133–1143. doi: 10.1083/jcb.200212046. [PMC free article] [PubMed] [CrossRef] [Google Scholar]
  • Chen CW, Corselli Yard, Peault B, Huard J. Human blood-vessel-derived stalk cells for tissue repair and regeneration. J Biomed Biotechnol. 2012;2012:597439. [PMC free article] [PubMed] [Google Scholar]
  • Collins CA. Satellite cell self-renewal. Curr Opin Pharmacol. 2006;six(three):301–306. doi: ten.1016/j.coph.2006.01.006. [PubMed] [CrossRef] [Google Scholar]
  • Cossu G, Sampaolesi K. New therapies for Duchenne muscular dystrophy: challenges, prospects and clinical trials. Trends Mol Med. 2007;thirteen(12):520–526. doi: 10.1016/j.molmed.2007.10.003. [PubMed] [CrossRef] [Google Scholar]
  • Cossu G, Previtali SC, Napolitano S, Cicalese MP, Tedesco FS, Nicastro F, Noviello 1000, Roostalu U, Natali Sora MG, Scarlato M, De Pellegrin Thousand, Godi C, Giuliani S, Ciotti F, Tonlorenzi R, Lorenzetti I, Rivellini C, Benedetti S, Gatti R, Marktel S, Mazzi B, Tettamanti A, Ragazzi M, Imro MA, Marano G, Ambrosi A, Fiori R, Sormani MP, Bonini C, Venturini M, Politi LS, Torrente Y, Ciceri F. Intra-arterial transplantation of HLA-matched donor mesoangioblasts in Duchenne muscular dystrophy. EMBO Mol Med. 2015 [PMC costless commodity] [PubMed] [Google Scholar]
  • Crane JD, Ogborn DI, Cupido C, Melov South, Hubbard A, Bourgeois JM, Tarnopolsky MA. Massage therapy attenuates inflammatory signaling subsequently exercise-induced muscle damage. Sci Transl Med. 2012;4(119):119ra113. doi: 10.1126/scitranslmed.3002882. [PubMed] [CrossRef] [Google Scholar]
  • Crisco JJ, Jokl P, Heinen GT, Connell MD, Panjabi MM. A muscle contusion injury model. Biomechanics, physiology, and histology. Am J Sports Med. 1994;22(five):702–710. doi: 10.1177/036354659402200521. [PubMed] [CrossRef] [Google Scholar]
  • Darby IA, Zakuan N, Billet F, Desmouliere A. The myofibroblast, a primal cell in normal and pathological tissue repair. Cell Mol Life Sci. 2016;73(6):1145–1157. doi: ten.1007/s00018-015-2110-0. [PubMed] [CrossRef] [Google Scholar]
  • Deasy BM, Feduska JM, Payne TR, Li Y, Ambrosio F, Huard J. Effect of VEGF on the regenerative capacity of muscle stalk cells in dystrophic skeletal muscle. Mol Ther. 2009;17(x):1788–1798. doi: 10.1038/mt.2009.136. [PMC free article] [PubMed] [CrossRef] [Google Scholar]
  • Desmouliere A, Gabbiani G. Myofibroblast differentiation during fibrosis. Exp Nephrol. 1995;3(2):134–139. [PubMed] [Google Scholar]
  • Dhawan J, Rando TA. Stem cells in postnatal myogenesis: molecular mechanisms of satellite cell quiescence, activation and replenishment. Trends Cell Biol. 2005;xv(12):666–673. doi: 10.1016/j.tcb.2005.10.007. [PubMed] [CrossRef] [Google Scholar]
  • Dumont NA, Bentzinger CF, Sincennes MC, Rudnicki MA. Satellite cells and skeletal muscle regeneration. Compr Physiol. 2015;5(3):1027–1059. doi: ten.1002/cphy.c140068. [PubMed] [CrossRef] [Google Scholar]
  • Dumont NA, Wang YX, Rudnicki MA. Intrinsic and extrinsic mechanisms regulating satellite cell office. Evolution. 2015;142(9):1572–1581. doi: 10.1242/dev.114223. [PMC complimentary article] [PubMed] [CrossRef] [Google Scholar]
  • Engebretsen L, Steffen K, Alsousou J, Anitua E, Bachl N, Devilee R, Everts P, Hamilton B, Huard J, Jenoure P, Kelberine F, Kon E, Maffulli North, Matheson G, Mei-Dan O, Menetrey J, Philippon Thousand, Randelli P, Schamasch P, Schwellnus M, Vernec A, Verrall G. IOC consensus newspaper on the utilize of platelet-rich plasma in sports medicine. Br J Sports Med. 2010;44(15):1072–1081. doi: x.1136/bjsm.2010.079822. [PubMed] [CrossRef] [Google Scholar]
  • Engert JC, Berglund EB, Rosenthal N. Proliferation precedes differentiation in IGF-I-stimulated myogenesis. J Cell Biol. 1996;135(2):431–440. doi: 10.1083/jcb.135.2.431. [PMC gratis article] [PubMed] [CrossRef] [Google Scholar]
  • Engler AJ, Sen S, Sweeney HL, Discher DE. Matrix elasticity directs stem cell lineage specification. Cell. 2006;126(iv):677–689. doi: 10.1016/j.cell.2006.06.044. [PubMed] [CrossRef] [Google Scholar]
  • Floss T, Arnold HH, Braun T. A function for FGF-half dozen in skeletal muscle regeneration. Genes Dev. 1997;11(xvi):2040–2051. doi: 10.1101/gad.xi.sixteen.2040. [PMC gratuitous article] [PubMed] [CrossRef] [Google Scholar]
  • Frey SP, Jansen H, Raschke MJ, Meffert RH, Ochman S. VEGF improves skeletal muscle regeneration afterward acute trauma and reconstruction of the limb in a rabbit model. Clin Orthop Relat Res. 2012;470(12):3607–3614. doi: 10.1007/s11999-012-2456-7. [PMC gratis article] [PubMed] [CrossRef] [Google Scholar]
  • Fukushima K, Badlani North, Usas A, Riano F, Fu F, Huard J. The use of an antifibrosis agent to improve muscle recovery after laceration. Am J Sports Med. 2001;29(iv):394–402. [PubMed] [Google Scholar]
  • Garg K, Corona BT, Walters TJ. Therapeutic strategies for preventing skeletal musculus fibrosis after injury. Front Pharmacol. 2015;half dozen:87. doi: ten.3389/fphar.2015.00087. [PMC free article] [PubMed] [CrossRef] [Google Scholar]
  • Garrett WE, Jr, Seaber AV, Boswick J, Urbaniak JR, Goldner JL. Recovery of skeletal musculus later on laceration and repair. J Hand Surg. 1984;nine(v):683–692. doi: 10.1016/S0363-5023(84)80014-iii. [PubMed] [CrossRef] [Google Scholar]
  • Gilbert PM, Havenstrite KL, Magnusson KE, Sacco A, Leonardi NA, Kraft P, Nguyen NK, Thrun S, Lutolf MP, Blau HM. Substrate elasticity regulates skeletal muscle stalk cell self-renewal in culture. Science. 2010;329(5995):1078–1081. doi: 10.1126/scientific discipline.1191035. [PMC free commodity] [PubMed] [CrossRef] [Google Scholar]
  • Grounds MD. Muscle regeneration: molecular aspects and therapeutic implications. Curr Opin Neurol. 1999;12(5):535–543. doi: x.1097/00019052-199910000-00007. [PubMed] [CrossRef] [Google Scholar]
  • Hamid MS, Yusof A, Mohamed Ali MR. Platelet-rich plasma (PRP) for acute muscle injury: a systematic review. PLoS I. 2014;ix(2) doi: 10.1371/journal.pone.0090538. [PMC free article] [PubMed] [CrossRef] [Google Scholar]
  • Hammond JW, Hinton RY, Scroll LA, Muriel JM, Lovering RM. Employ of autologous platelet-rich plasma to care for muscle strain injuries. Am J Sports Med. 2009;37(vi):1135–1142. doi: 10.1177/0363546508330974. [PMC complimentary article] [PubMed] [CrossRef] [Google Scholar]
  • Colina East, Boontheekul T, Mooney DJ. Designing scaffolds to raise transplanted myoblast survival and migration. Tissue Eng. 2006;12(5):1295–1304. doi: 10.1089/x.2006.12.1295. [PubMed] [CrossRef] [Google Scholar]
  • Huard J, Li Y, Fu FH. Muscle injuries and repair: current trends in research. J Bone Articulation Surg Am. 2002;84-A(5):822–832. [PubMed] [Google Scholar]
  • Hurme T, Kalimo H. Activation of myogenic precursor cells after muscle injury. Med Sci Sports Exerc. 1992;24(2):197–205. doi: x.1249/00005768-199202000-00007. [PubMed] [CrossRef] [Google Scholar]
  • Hwang OK, Park JK, Lee EJ, Lee EM, Kim AY, Jeong KS. Therapeutic upshot of losartan, an angiotensin II type 1 receptor antagonist, on CCl(4)-induced skeletal muscle injury. Int J Mol Sci. 2016;17(2):227. doi: 10.3390/ijms17020227. [PMC free article] [PubMed] [CrossRef] [Google Scholar]
  • Jarvinen TA, Jarvinen TL, Kaariainen K, Kalimo H, Jarvinen Chiliad. Muscle injuries: biology and treatment. Am J Sports Med. 2005;33(5):745–764. doi: ten.1177/0363546505274714. [PubMed] [CrossRef] [Google Scholar]
  • Jeon OH, Elisseeff J. Orthopedic tissue regeneration: cells, scaffolds, and modest molecules. Drug Deliv Transl Res. 2016;half dozen(2):105–120. doi: 10.1007/s13346-015-0266-7. [PubMed] [CrossRef] [Google Scholar]
  • Karvinen H, Pasanen E, Rissanen TT, Korpisalo P, Vahakangas E, Jazwa A, Giacca Thou, Yla-Herttuala S. Long-term VEGF-A expression promotes abnormal angiogenesis and fibrosis in skeletal muscle. Gene Ther. 2011;18(12):1166–1172. doi: 10.1038/gt.2011.66. [PubMed] [CrossRef] [Google Scholar]
  • Kasemkijwattana C, Menetrey J, Somogyl Chiliad, Moreland MS, Fu FH, Buranapanitkit B, Watkins SC, Huard J. Development of approaches to better the healing following musculus contusion. Cell Transplant. 1998;vii(6):585–598. doi: x.1016/S0963-6897(98)00037-two. [PubMed] [CrossRef] [Google Scholar]
  • Kasemkijwattana C, Menetrey J, Bosch P, Somogyi Grand, Moreland MS, Fu FH, Buranapanitkit B, Watkins SS, Huard J. Use of growth factors to improve muscle healing after strain injury. Clin Orthop. 2000;370:272–285. doi: 10.1097/00003086-200001000-00028. [PubMed] [CrossRef] [Google Scholar]
  • Kastner Southward, Elias MC, Rivera AJ, Yablonka-Reuveni Z. Gene expression patterns of the fibroblast growth factors and their receptors during myogenesis of rat satellite cells. J Histochem Cytochem. 2000;48(viii):1079–1096. doi: ten.1177/002215540004800805. [PubMed] [CrossRef] [Google Scholar]
  • Kumar A, Chaudhry I, Reid MB, Boriek AM. Distinct signaling pathways are activated in response to mechanical stress applied axially and transversely to skeletal muscle fibers. J Biol Chem. 2002;277(48):46493–46503. doi: 10.1074/jbc.M203654200. [PubMed] [CrossRef] [Google Scholar]
  • Constabulary PK, Bertorini TE, Goodwin TG, Chen M, Fang QW, Li HJ, Kirby DS, Florendo JA, Herrod HG, Golden GS. Dystrophin production induced by myoblast transfer therapy in Duchenne muscular dystrophy. Lancet. 1990;336(8707):114–115. doi: x.1016/0140-6736(ninety)91628-Due north. [PubMed] [CrossRef] [Google Scholar]
  • Lee C, Fukushima Thousand, Usas A, Xin 50, Pelinkovic D, Martinek V, Huard J. Biological intervention based on cell and gene therapy to improve muscle healing later laceration. J Musculoskelet Res. 2000;iv(4):256–277. doi: 10.1142/S0218957700000264. [CrossRef] [Google Scholar]
  • Lehto MU, Jarvinen MJ. Muscle injuries, their healing procedure and handling. Ann Chir Gynaecol. 1991;80(two):102–108. [PubMed] [Google Scholar]
  • Lehto K, Sims TJ, Bailey AJ. Skeletal muscle injury--molecular changes in the collagen during healing. Res Exp Med. 1985;185(2):95–106. doi: 10.1007/BF01854894. [PubMed] [CrossRef] [Google Scholar]
  • Lemos DR, Babaeijandaghi F, Low Yard, Chang CK, Lee ST, Fiore D, Zhang RH, Natarajan A, Nedospasov SA, Rossi FM. Nilotinib reduces muscle fibrosis in chronic muscle injury by promoting TNF-mediated apoptosis of fibro/adipogenic progenitors. Nat Med. 2015;21(vii):786–794. doi: 10.1038/nm.3869. [PubMed] [CrossRef] [Google Scholar]
  • Li Y, Huard J. Differentiation of muscle-derived cells into myofibroblasts in injured skeletal muscle. Am J Pathol. 2002;161(3):895–907. doi: 10.1016/S0002-9440(10)64250-2. [PMC free commodity] [PubMed] [CrossRef] [Google Scholar]
  • Li Y, Foster W, Deasy BM, Chan Y, Prisk V, Tang Y, Cummins J, Huard J. Transforming growth factor-beta1 induces the differentiation of myogenic cells into fibrotic cells in injured skeletal muscle: a primal issue in muscle fibrogenesis. Am J Pathol. 2004;164(3):1007–1019. doi: 10.1016/S0002-9440(10)63188-4. [PMC complimentary article] [PubMed] [CrossRef] [Google Scholar]
  • Li Y, Li J, Zhu J, Sun B, Branca M, Tang Y, Foster W, Xiao X, Huard J. Decorin factor transfer promotes muscle prison cell differentiation and muscle regeneration. Mol Ther. 2007;fifteen(9):1616–1622. doi: x.1038/sj.mt.6300250. [PubMed] [CrossRef] [Google Scholar]
  • Li H, Hicks JJ, Wang 50, Oyster N, Philippon MJ, Hurwitz S, Hogan MV, Huard J. Customized platelet-rich plasma with transforming growth factor beta1 neutralization antibody to reduce fibrosis in skeletal muscle. Biomaterials. 2016;87:147–156. doi: ten.1016/j.biomaterials.2016.02.017. [PubMed] [CrossRef] [Google Scholar]
  • Lipton BH, Schultz E. Developmental fate of skeletal muscle satellite cells. Scientific discipline. 1979;205(4412):1292–1294. doi: x.1126/science.472747. [PubMed] [CrossRef] [Google Scholar]
  • Mann CJ, Perdiguero Due east, Kharraz Y, Aguilar S, Pessina P, Serrano AL, Munoz-Canoves P. Aberrant repair and fibrosis development in skeletal muscle. Skelet Muscle. 2011;1(1):21. doi: x.1186/2044-5040-1-21. [PMC complimentary article] [PubMed] [CrossRef] [Google Scholar]
  • McLennan IS. Degenerating and regenerating skeletal muscles incorporate several subpopulations of macrophages with singled-out spatial and temporal distributions. J Anat. 1996;188(Pt 1):17–28. [PMC free commodity] [PubMed] [Google Scholar]
  • Mendell JR, Kissel JT, Amato AA, Male monarch W, Signore L, Prior TW, Sahenk Z, Benson South, McAndrew PE, Rice R, Nagaraja H, Stephens R, Lantry L, Morris GE, Burghes AH. Myoblast transfer in the treatment of Duchenne'south muscular dystrophy. Due north Engl J Med. 1995;333(xiii):832–838. doi: ten.1056/NEJM199509283331303. [PubMed] [CrossRef] [Google Scholar]
  • Menetrey J, Kasemkijwattana C, Fu FH, Moreland MS, Huard J. Suturing versus immobilization of a muscle laceration. A morphological and functional report in a mouse model. Am J Sports Med. 1999;27(two):222–229. [PubMed] [Google Scholar]
  • Menetrey J, Kasemkijwattana C, Day CS, Bosch P, Vogt Grand, Fu FH, Moreland MS, Huard J. Growth factors improve muscle healing in vivo. J Bone Joint Surg Br. 2000;82(1):131–137. doi: 10.1302/0301-620X.82B1.8954. [PubMed] [CrossRef] [Google Scholar]
  • Meng J, Chun S, Asfahani R, Lochmuller H, Muntoni F, Morgan J. Human skeletal muscle-derived CD133(+) cells grade functional satellite cells afterwards intramuscular transplantation in immunodeficient host mice. Mol Ther. 2014;22(5):1008–1017. doi: x.1038/mt.2014.26. [PMC gratuitous commodity] [PubMed] [CrossRef] [Google Scholar]
  • Messina Due south, Mazzeo A, Bitto A, Aguennouz Chiliad, Migliorato A, De Pasquale MG, Minutoli L, Altavilla D, Zentilin Fifty, Giacca M, Squadrito F, Vita G. VEGF overexpression via adeno-associated virus gene transfer promotes skeletal musculus regeneration and enhances muscle part in mdx mice. FASEB J. 2007;21(xiii):3737–3746. doi: ten.1096/fj.07-8459com. [PubMed] [CrossRef] [Google Scholar]
  • Miller KJ, Thaloor D, Matteson Due south, Pavlath GK. Hepatocyte growth factor affects satellite cell activation and differentiation in regenerating skeletal muscle. Am J Physiol Jail cell Physiol. 2000;278(one):C174–C181. [PubMed] [Google Scholar]
  • Mourkioti F, Rosenthal Northward. IGF-1, inflammation and stem cells: interactions during musculus regeneration. Trends Immunol. 2005;26(10):535–542. doi: 10.1016/j.information technology.2005.08.002. [PubMed] [CrossRef] [Google Scholar]
  • Munoz-Canoves P, Serrano AL. Macrophages determine between regeneration and fibrosis in muscle. Trends Endocrinol Metab. 2015;26(9):449–450. doi: 10.1016/j.tem.2015.07.005. [PubMed] [CrossRef] [Google Scholar]
  • Musaro A, McCullagh KJ, Naya FJ, Olson EN, Rosenthal N. IGF-1 induces skeletal myocyte hypertrophy through calcineurin in association with GATA-ii and NF-ATc1. Nature. 1999;400(6744):581–585. doi: 10.1038/23060. [PubMed] [CrossRef] [Google Scholar]
  • Musaro A, McCullagh G, Paul A, Houghton L, Dobrowolny K, Molinaro M, Barton ER, Sweeney HL, Rosenthal N. Localized Igf-1 transgene expression sustains hypertrophy and regeneration in senescent skeletal muscle. Nat Genet. 2001;27(2):195–200. doi: ten.1038/84839. [PubMed] [CrossRef] [Google Scholar]
  • Musaro A, Giacinti C, Borsellino 1000, Dobrowolny G, Pelosi Fifty, Cairns L, Ottolenghi Due south, Cossu G, Bernardi Yard, Battistini 50, Molinaro G, Rosenthal N. Stem jail cell-mediated muscle regeneration is enhanced past local isoform of insulin-like growth cistron ane. Proc Natl Acad Sci U South A. 2004;101(5):1206–1210. doi: x.1073/pnas.0303792101. [PMC free commodity] [PubMed] [CrossRef] [Google Scholar]
  • Ota S, Uehara K, Nozaki M, Kobayashi T, Terada Due south, Tobita K, Fu FH, Huard J. Intramuscular transplantation of muscle-derived stalk cells accelerates skeletal muscle healing after contusion injury via enhancement of angiogenesis. Am J Sports Med. 2011;39(9):1912–1922. doi: x.1177/0363546511415239. [PubMed] [CrossRef] [Google Scholar]
  • Park JK, Ki MR, Lee EM, Kim AY, You SY, Han SY, Lee EJ, Hong IH, Kwon SH, Kim SJ, Rando TA, Jeong KS. Losartan improves adipose tissue-derived stem cell niche by inhibiting transforming growth gene-beta and fibrosis in skeletal muscle injury. Cell Transplant. 2012;21(11):2407–2424. doi: ten.3727/096368912X637055. [PubMed] [CrossRef] [Google Scholar]
  • Partridge TA, Morgan JE, Coulton GR, Hoffman EP, Kunkel LM. Conversion of mdx myofibres from dystrophin-negative to -positive by injection of normal myoblasts. Nature. 1989;337(6203):176–179. doi: 10.1038/337176a0. [PubMed] [CrossRef] [Google Scholar]
  • Powell CA, Smiley BL, Mills J, Vandenburgh HH. Mechanical stimulation improves tissue-engineered human skeletal muscle. Am J Physiol Cell Physiol. 2002;283(v):C1557–C1565. doi: 10.1152/ajpcell.00595.2001. [PubMed] [CrossRef] [Google Scholar]
  • Proto JD, Tang Y, Lu A, Chen WC, Stahl E, Poddar Grand, Beckman SA, Robbins PD, Nidernhofer LJ, Imbrogno 1000, Hannigan T, Mars WM, Wang B, Huard J. NF-kappaB inhibition reveals a novel role for HGF during skeletal musculus repair. Jail cell Death Dis. 2015;half-dozen doi: ten.1038/cddis.2015.66. [PMC free article] [PubMed] [CrossRef] [Google Scholar]
  • Rantanen J, Ranne J, Hurme T, Kalimo H. Denervated segments of injured skeletal muscle fibers are reinnervated past newly formed neuromuscular junctions. J Neuropathol Exp Neurol. 1995;54(ii):188–194. doi: 10.1097/00005072-199503000-00005. [PubMed] [CrossRef] [Google Scholar]
  • Relaix F, Zammit PS. Satellite cells are essential for skeletal musculus regeneration: the jail cell on the edge returns centre phase. Development. 2012;139(16):2845–2856. doi: 10.1242/dev.069088. [PubMed] [CrossRef] [Google Scholar]
  • Reurink Yard, Goudswaard GJ, Moen MH, Weir A, Verhaar JA, Bierma-Zeinstra SM, Maas 1000, Tol JL, Dutch Hamstring Injection Therapy Study I Platelet-rich plasma injections in astute muscle injury. N Engl J Med. 2014;370(26):2546–2547. doi: x.1056/NEJMc1402340. [PubMed] [CrossRef] [Google Scholar]
  • Reurink G, Goudswaard GJ, Moen MH, Weir A, Verhaar JA, Bierma-Zeinstra SM, Maas M, Tol JL, Dutch HITsI Rationale, secondary outcome scores and i-twelvemonth follow-up of a randomised trial of platelet-rich plasma injections in acute hamstring muscle injury: the Dutch Hamstring Injection Therapy study. Br J Sports Med. 2015;49(18):1206–1212. doi: 10.1136/bjsports-2014-094250. [PubMed] [CrossRef] [Google Scholar]
  • Rocheteau P, Vinet G, Chretien F. Dormancy and quiescence of skeletal muscle stem cells. Results Probl Cell Differ. 2015;56:215–235. doi: ten.1007/978-3-662-44608-9_10. [PubMed] [CrossRef] [Google Scholar]
  • Sadtler 1000, Estrellas K, Allen BW, Wolf MT, Fan H, Tam AJ, Patel CH, Luber BS, Wang H, Wagner KR, Powell JD, Housseau F, Pardoll DM, Elisseeff JH. Developing a pro-regenerative biomaterial scaffold microenvironment requires T helper 2 cells. Science. 2016;352(6283):366–370. doi: x.1126/scientific discipline.aad9272. [PMC free commodity] [PubMed] [CrossRef] [Google Scholar]
  • Saera-Vila A, Kish PE, Kahana A. Fgf regulates dedifferentiation during skeletal muscle regeneration in adult zebrafish. Cell Signal. 2016;28(nine):1196–1204. doi: 10.1016/j.cellsig.2016.06.001. [PMC complimentary article] [PubMed] [CrossRef] [Google Scholar]
  • Sambasivan R, Yao R, Kissenpfennig A, Van Wittenberghe L, Paldi A, Gayraud-Morel B, Guenou H, Malissen B, Tajbakhsh Southward, Galy A. Pax7-expressing satellite cells are indispensable for developed skeletal muscle regeneration. Evolution. 2011;138(17):3647–3656. doi: x.1242/dev.067587. [PubMed] [CrossRef] [Google Scholar]
  • Sampaolesi 1000, Absorb S, D'Antona G, Granger N, Tonlorenzi R, Innocenzi A, Mognol P, Thibaud JL, Galvez BG, Barthelemy I, Perani L, Mantero Southward, Guttinger M, Pansarasa O, Rinaldi C, Cusella De Angelis MG, Torrente Y, Bordignon C, Bottinelli R, Cossu G. Mesoangioblast stem cells improve muscle function in dystrophic dogs. Nature. 2006;444(7119):574–579. doi: ten.1038/nature05282. [PubMed] [CrossRef] [Google Scholar]
  • Schiaffino Southward, Mammucari C. Regulation of skeletal muscle growth by the IGF1-Akt/PKB pathway: insights from genetic models. Skelet Musculus. 2011;1(i):4. doi: 10.1186/2044-5040-1-4. [PMC gratuitous article] [PubMed] [CrossRef] [Google Scholar]
  • Scholz D, Thomas Southward, Sass S, Podzuweit T. Angiogenesis and myogenesis as two facets of inflammatory post-ischemic tissue regeneration. Mol Cell Biochem. 2003;246(1-ii):57–67. doi: 10.1023/A:1023403928385. [PubMed] [CrossRef] [Google Scholar]
  • Sheehan SM, Tatsumi R, Temm-Grove CJ, Allen RE. HGF is an autocrine growth factor for skeletal muscle satellite cells in vitro. Musculus Nerve. 2000;23(2):239–245. doi: x.1002/(SICI)1097-4598(200002)23:2<239::AID-MUS15>3.0.CO;ii-U. [PubMed] [CrossRef] [Google Scholar]
  • Skuk D, Goulet M, Roy B, Piette Five, Cote CH, Chapdelaine P, Hogrel JY, Paradis M, Bouchard JP, Sylvain M, Lachance JG, Tremblay JP. First test of a "high-density injection" protocol for myogenic jail cell transplantation throughout large volumes of muscles in a Duchenne muscular dystrophy patient: 18 months follow-upward. Neuromuscul Disord. 2007;17(1):38–46. doi: 10.1016/j.nmd.2006.ten.003. [PubMed] [CrossRef] [Google Scholar]
  • Taniguti AP, Pertille A, Matsumura CY, Santo Neto H, Marques MJ. Prevention of musculus fibrosis and myonecrosis in mdx mice by suramin, a TGF-beta1 blocker. Musculus Nerve. 2011;43(1):82–87. doi: 10.1002/mus.21869. [PubMed] [CrossRef] [Google Scholar]
  • Tatsumi R, Sheehan SM, Iwasaki H, Hattori A, Allen RE. Mechanical stretch induces activation of skeletal muscle satellite cells in vitro. Exp Cell Res. 2001;267(1):107–114. doi: 10.1006/excr.2001.5252. [PubMed] [CrossRef] [Google Scholar]
  • Tedesco FS, Cossu Thousand. Stalk cell therapies for muscle disorders. Curr Opin Neurol. 2012;25(v):597–603. doi: 10.1097/WCO.0b013e328357f288. [PubMed] [CrossRef] [Google Scholar]
  • Tedesco FS, Dellavalle A, Diaz-Manera J, Messina 1000, Cossu 1000. Repairing skeletal muscle: regenerative potential of skeletal muscle stem cells. J Clin Invest. 2010;120(1):11–nineteen. doi: ten.1172/JCI40373. [PMC complimentary commodity] [PubMed] [CrossRef] [Google Scholar]
  • Terada S, Ota S, Kobayashi M, Kobayashi T, Mifune Y, Takayama K, Witt 1000, Vadala G, Oyster North, Otsuka T, Fu FH, Huard J. Use of an antifibrotic amanuensis improves the effect of platelet-rich plasma on muscle healing after injury. J Bone Joint Surg Am. 2013;95(xi):980–988. doi: x.2106/JBJS.Fifty.00266. [PubMed] [CrossRef] [Google Scholar]
  • Tidball JG. Inflammatory cell response to astute muscle injury. Med Sci Sports Exerc. 1995;27(vii):1022–1032. doi: 10.1249/00005768-199507000-00011. [PubMed] [CrossRef] [Google Scholar]
  • Tidball JG. Inflammatory processes in musculus injury and repair. Am J Physiol Regul Integr Comp Physiol. 2005;288(2):R345–R353. doi: 10.1152/ajpregu.00454.2004. [PubMed] [CrossRef] [Google Scholar]
  • Tidball JG. Mechanisms of muscle injury, repair, and regeneration. Compr Physiol. 2011;1(four):2029–2062. [PubMed] [Google Scholar]
  • Tidball JG, Wehling-Henricks M. Macrophages promote musculus membrane repair and musculus fibre growth and regeneration during modified muscle loading in mice in vivo. J Physiol. 2007;578(Pt one):327–336. doi: ten.1113/jphysiol.2006.118265. [PMC costless article] [PubMed] [CrossRef] [Google Scholar]
  • Tidball JG, Welc SS. Macrophage-Derived IGF-ane Is a Potent Coordinator of Myogenesis and Inflammation in Regenerating Muscle. Mol Ther. 2015;23(7):1134–1135. doi: x.1038/mt.2015.97. [PMC free article] [PubMed] [CrossRef] [Google Scholar]
  • Toumi H, Best TM. The inflammatory response: friend or enemy for muscle injury? Br J Sports Med. 2003;37(4):284–286. doi: ten.1136/bjsm.37.4.284. [PMC free article] [PubMed] [CrossRef] [Google Scholar]
  • Vaittinen S, Lukka R, Sahlgren C, Hurme T, Rantanen J, Lendahl U, Eriksson JE, Kalimo H. The expression of intermediate filament protein nestin as related to vimentin and desmin in regenerating skeletal muscle. J Neuropathol Exp Neurol. 2001;lx(vi):588–597. doi: 10.1093/jnen/lx.half dozen.588. [PubMed] [CrossRef] [Google Scholar]
  • Walczak Exist, Johnson CN, Howe BM. Myositis Ossificans. J Am Acad Orthop Surg. 2015;23(10):612–622. doi: 10.5435/JAAOS-D-14-00269. [PubMed] [CrossRef] [Google Scholar]
  • Wu H, Xiong WC, Mei Fifty. To build a synapse: signaling pathways in neuromuscular junction assembly. Development. 2010;137(vii):1017–1033. doi: x.1242/dev.038711. [PMC free article] [PubMed] [CrossRef] [Google Scholar]
  • Yablonka-Reuveni Z, Balestreri TM, Bowen-Pope DF. Regulation of proliferation and differentiation of myoblasts derived from adult mouse skeletal muscle past specific isoforms of PDGF. J Cell Biol. 1990;111(4):1623–1629. doi: 10.1083/jcb.111.4.1623. [PMC gratuitous commodity] [PubMed] [CrossRef] [Google Scholar]
  • Yin H, Price F, Rudnicki MA. Satellite cells and the muscle stem cell niche. Physiol Rev. 2013;93(1):23–67. doi: 10.1152/physrev.00043.2011. [PMC free article] [PubMed] [CrossRef] [Google Scholar]
  • Zhao W, Lu H, Wang Ten, Ransohoff RM, Zhou L. CX3CR1 deficiency delays acute skeletal muscle injury repair past impairing macrophage functions. FASEB J. 2016;30(i):380–393. doi: 10.1096/fj.14-270090. [PMC free article] [PubMed] [CrossRef] [Google Scholar]
  • Zheng B, Cao B, Crisan M, Sun B, Li G, Logar A, Yap S, Pollett JB, Drowley L, Cassino T, Gharaibeh B, Deasy BM, Huard J, Peault B. Prospective identification of myogenic endothelial cells in human skeletal muscle. Nat Biotechnol. 2007;25(9):1025–1034. doi: x.1038/nbt1334. [PubMed] [CrossRef] [Google Scholar]

Source: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4958098/

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