How Does Muscle Tissue Repair Itself

J Exp Orthop. 2022 Dec; three: 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 14, Switzerland

Jacques Menetrey

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

Received 2022 Mar 15; Accepted 2022 Jul 15.

Abstract

Satellite cells are tissue resident muscle stem cells required for postnatal skeletal musculus growth and repair through replacement of damaged myofibers. Muscle regeneration is coordinated through dissimilar mechanisms, which imply jail cell-cell and cell-matrix interactions besides every bit extracellular secreted factors. Cellular dynamics during musculus regeneration are highly complex. Immune, fibrotic, vascular and myogenic cells appear with distinct temporal and spatial kinetics afterward musculus injury. Three primary phases accept been identified in the process of muscle regeneration; a destruction stage 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 small musculus injuries, such every bit strains, heal spontaneously, severe muscle injuries class fibrotic tissue that impairs musculus part and atomic number 82 to muscle contracture and chronic hurting. Current therapeutic approaches accept limited effectiveness and optimal strategies for such lesions are non known notwithstanding. Various strategies, including growth factors injections, transplantation of muscle stalk cells in combination or not with biological scaffolds, anti-fibrotic therapies and mechanical stimulation, may become therapeutic alternatives to improve functional muscle recovery.

Keywords: Skeletal muscle, Injury, Regeneration, Stem cell, Fibrosis, Scaffolds, Growth factors

Introduction

Human skeletal muscle is about 40 % of the body mass and is formed by bundle 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 subsequently injury (Hurme and Kalimo 1992; Lipton and Schultz 1979) (Sambasivan et al. 2022; Dumont et al. 2022a). In adult muscles, SC are found in a quiescent land and represent, depending on species, historic period, muscle location, and muscle type, around five to 10 % of skeletal muscle cells (Rocheteau et al. 2022). After injury, SC go activated, proliferate and give ascent 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 multifariousness of events, including straight trauma such equally muscle lacerations and contusions, indirect insults such as strains and also from degenerative diseases such as 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 as strain. In contrast, after astringent injuries, muscle healing is incomplete, often resulting in the formation of fibrotic tissue that impairs muscle function. Although researchers accept extensively investigated various approaches to improve muscle healing, there is still no gold standard treatment.

This concise review provides a sight about the various phases of muscle repair and regeneration, namely degeneration, inflammation, regeneration, remodeling and maturation. We also give an overview of enquiry efforts that accept focused on the utilise of stem cell therapy, growth factors and/or biological scaffolds to ameliorate muscle regeneration and repair. We also accost the therapeutic potential of mechanical stimulation and of anti-fibrotic therapy to enhance muscle regeneration and repair.

Review

Musculus healing process

Skeletal muscle has a robust innate capability for repair after injury through the presence of adult musculus stalk cells known as satellite cells (SC). The disruption of muscle tissue homeostasis, caused by injury, generates sequential involvement of various players effectually three primary phases (Fig.1).

(1, two) Degeneration/inflammation phase: characterized past rupture and necrosis of the myofibers, formation of a hematoma and an of import inflammatory reaction.
(3) Regeneration phase: phagocytosis of damaged tissue, followed past myofibers regeneration, leading to satellite cell activation.
(4, 5) Remodeling phase: maturation of regenerated myofibers with recovery of muscle functional capacity (four) and also fibrosis and scar tissue formation (5).

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

Muscle degeneration and inflammation

Active musculus degeneration and inflammation occur inside the offset few days after injury. The initial consequence is necrosis of the musculus fibers, which is triggered by disruption of local homeostasis and particularly past unregulated influx of calcium through sarcolemma lesions (Tidball 2022). Backlog in cytoplasmic calcium causes proteases and hydrolases activation that contribute to musculus damage and also causes activation of enzymes that drive the product of mitogenic substances for muscle and allowed cells (Tidball 2005). Later musculus degeneration, neutrophils are the first inflammatory cells infiltrating the lesion. A large number of pro-inflammatory molecules such as cytokines (TNF-α, IL-6), chemokine (CCL17, CCL2) and growth factors (FGF, HGF, IGF-I, VEGF; TGF-β1) are secreted by neutrophils in social club 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 announced sequentially during muscle repair (Arnold et al. 2007). M1 macrophages, defined as pro-inflammatory macrophages, act during the first few days after injury,. contribute to cell lysis, removal of cellular droppings and stimulate myoblast proliferation. Conversely, M2 macrophages, defined every bit anti-inflammatory macrophages, act 2 to 4 days after injury, attenuate the inflammatory response and favor musculus repair past promoting myotubes formation (Tidball and Wehling-Henricks 2007; Chazaud 2022; Chazaud et al. 2003). Macrophages, infiltrating injured muscle, are fundamental players of the healing process (Zhao et al. 2022), able to participate in the musculus regeneration process or to favor fibrosis (Munoz-Canoves and Serrano 2022; Lemos et al. 2022).

Muscle regeneration, remodeling and maturation

Muscle regeneration ordinarily starts during the first 4–v days afterwards injury, peaks at 2 weeks, and and so gradually diminishes 3 to 4 weeks later injury. It's a multiple steps process including activation/proliferation of SC, repair and maturation of damaged muscle fibers and connective tissue formation. A fine residuum between these mechanisms is essential for a total recovery of the contractile muscle function.

Muscle fibers are post-mitotic cells, which do not have the capacity to divide. Post-obit an injury, damaged muscle fibers can't be repaired without the presence of adult muscle stem cells, the satellite cells (SC) (Relaix and Zammit 2022; Sambasivan et al. 2022). Following activation, SC proliferate and generate a population of myoblasts that can either differentiate to repair damaged fibers or, for a modest proportion, self-renew to maintain the SC pool for possible futurity demands of muscle regeneration (Collins 2006; Dhawan and Rando 2005). SC bike progression and jail cell fate determination are control past circuitous regulatory mechanisms in which, intrinsic and extrinsic factors are involved (Dumont et al. 2022a; Dumont et al. 2022b).

Connective tissue/fibrosis

Connective tissue remodeling is an important step of the regenerative muscle process. Chop-chop later on muscle injury, a gap is formed betwixt damaged musculus fibers and filled with a hematoma. Muscle injuries can be clinically classified depending of the nature of the hematoma (size, location). Tardily elimination of the hematoma is known to delay skeletal muscle regeneration, to improve fibrosis and to reduce biomechanical properties of the healing musculus (Beiner et al. 1999). In rare complication, major musculus injuries may atomic number 82 to the development of myositis ossificans that will impair muscle regeneration and repair (Beiner and Jokl 2002) (Walczak et al. 2022).

The presence of fibrin and fibronectin at the injury site, initiate the germination of an extracellular matrix that is rapidly invaded by fibroblasts (Darby et al. 2022; Desmouliere and Gabbiani 1995). Fibrogenic cytokines such as transforming growth factor β1 (TGF-β1) participate to excessive fibroblasts/myofibroblasts proliferation and to an increment in type I/III collagens, laminin and fibronectin production (Lehto et al. 1985). In its initial phase, the fibrotic response is beneficial, stabilizing the tissue and acting as a scaffold for myofibers regeneration. Nevertheless, an excessive collagen synthesis mail service injury, oftentimes outcome in an increase of scar tissue size over time that can prevent normal muscle function (Mann et al. 2022). Many growth factors are involved in the development of fibrosis, such as Connective Tissue Growth Factor (CTGF), Platelet-Derived Growth Factor (PDGF) or myostatin. TGF-β1, by stimulating fibroblasts/myofibroblasts to produce extracellular proteins such as fibronectin and type I/Iii collagen, has been identified as the cardinal element in this process (Mann et al. 2022),. Although fibroblasts are the major collagen-producing cells in skeletal muscle, TGF-β1 have besides an upshot directly on myoblasts causing their conversion to myofibroblasts. Thus myoblasts initially interim to repair damaged myofibers, will produce significant 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 muscle is one of the outset signs of musculus regeneration and is essential to its success. Without revascularization, muscle regeneration is incomplete and a significant fibrosis occurs (Best et al. 2022; Ota et al. 2022). Afterwards muscle trauma, blood vessels rupture induces tissue hypoxia at the injury site (Jarvinen et al. 2005). New capillaries formation rapidly after injury is therefore necessary (Scholz et al. 2003) for a functional muscle recovery. Secretion of angiogenic factors such every bit vascular endothelial growth factor (VEGF) at the lesion site is important and several studies have shown that VEGF, by favoring angiogenesis, improve skeletal muscle repair (Deasy et al. 2009; Frey et al. 2022).

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 accept place 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. Within 2–iii weeks afterwards muscle damage, the presence of newly formed NMJ is observed in regenerative muscle (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 cell types present at the inflammatory site, are release in the extracellular infinite and modulate the regenerative response (Tabular arrayi). Although hepatocyte growth factor (HGF), fibroblast growth cistron (FGF) and platelet-derived growth cistron (PDGF) are of involvement considering of their chapters to stimulate satellite cells (Sheehan et al. 2000; Allen and Boxhorn 1989; Yablonka-Reuveni et al. 1990), insulin like growth factor-1 (IGF-I) appears to be of particular importance for the muscle regeneration procedure. IGF-I stimulates myoblasts proliferation and differentiation (Engert et al. 1996) and is implicated in the regulation of muscle growth (Schiaffino and Mammucari 2022). In a mouse model, straight injections of man recombinant IGF-I at ii, v, and vii days after injury enhanced musculus healing in lacerated, contused, and strain-injured muscles (Menetrey et al. 2000; Kasemkijwattana et al. 2000). However, the efficacy of directly injection of recombinant proteins is express by the high concentration of the cistron typically required to elicit a measurable issue. This is mainly due to the bloodstream's rapid clearance of these molecules and their relatively short biological half-lives. Gene therapy may be an effective method past which to deliver high, maintainable concentrations of growth factor to injured muscle (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 within the lacerated site, despite high level of IGF-I production (Lee et al. 2000). Some other growth factor, VEGF, past favoring angiogenesis, is known to enhance skeletal muscle repair (Deasy et al. 2009; Frey et al. 2022; 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 every bit a possible alternative approach based on the power of autologous growth factors to meliorate skeletal muscle regeneration (Hamid et al. 2022; Hammond et al. 2009). Considered as safe products, autologous PRP injections are increasingly used in patients with sports-related injuries (Engebretsen et al. 2010). Notwithstanding, a recent randomized clinical trial show no significant positive effects of PRP injections, as compared with placebo injections, in patients with muscle injuries, upward to one year after injections (Reurink et al. 2022; Reurink et al. 2022). Customization of PRP preparation, equally 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. 2022).

Tabular array i

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 outcome of IGF-1 (Barton-Davis et al. 1999) - Serial injections of IGF-ane improve musculus healing in vivo (Menetrey et al. 2000). - Existence of a muscle specific isoform of IGF-i (mIGF-1) (Musaro et al. 1999; Musaro et al. 2004)	- Chemotactic for fibroblasts, increase collagen production, enhance fibrosis development	- IGF-i play a primal role in the enhancement of muscle regeneration- - Anti-inflammatory actions of IGF-i (Mourkioti and Rosenthal 2005; Tidball and Welc 2022)
HGF	- Promote myoblast proliferation and inhibit myoblast differentiation (Anderson 2022; Yin et al. 2022) - Of import role for satellite prison cell activation. Balance between the activation of satellite cells and their return to quiescence. (Chazaud 2010) - Recently, information technology was shown that a 2nd set of HGF production is crucial for inflammation resolution subsequently injury (Proto et al. 2022)	- Injection of HGF into injured muscle increased myoblast numbers only blocked the regeneration process (Miller et al. 2000)	- HGF is of import during the early phase of muscle regeneration, actuate satellite cells
VEGF	- Of import signaling protein that favor angiogenesis. - Promote myoblast migration, proliferation and survival. (Arsic et al. 2004) - VEGF assistants improves muscle regeneration. (Messina et al. 2007; Deasy et al. 2009)	- Non regulated VEGF expression promote abnormal angiogenesis and fibrosis in skeletal muscle (Karvinen et al. 2022)	- Importance of the proximity betwixt satellite cells and the microvasculature during musculus regeneration, role of VEGF
FGF	- Large family of mitogen involved in prison cell growth and survival - FGF-half-dozen has a muscle specific expression, stimulates satellite cell proliferation and promotes myogenic terminal differentiation (Floss et al. 1997) - FGF-2 promote satellite cell proliferation and inhibit myogenic differentiation (Menetrey et al. 2000; Kastner et al. 2000)	- Stimulate fibroblast proliferation,	- FGF signaling plays a primal role in muscle repair, blocking FGF signaling delay muscle regeneration (Saera-Vila et al. 2022).
TGF-β1	- Primal regulator of the balance 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. 2022).	- Anti fibrotic therapy past blocking overexpression of TGF-β1 amend musculus regeneration. (Burks et al. 2022; Hwang et al. 2022)
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 (Accuse and Rudnicki 2004)	- Stiff mitogen for fibroblasts	- Release from injured vessels and platelets, PDGF stimulates early on skeletal musculus regeneration

Stem cells

Transplantation of satellite cell-derived myoblasts has long been explored equally a promising approach for treatment 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 homo myoblasts were injected intramuscularly several times in dystrophic young boys muscles, accept not been successful (Law et al. 1990; Mendell et al. 1995). Fifty-fifty recently, despite articulate improvement in methodologies that raise the success of myoblast transplantation in Duchenne patients (Skuk et al. 2007), outcomes of clinical trials are still disappointing. These experiments have raised concerns virtually the express migratory and proliferative capacities of homo myoblasts, as well equally their limited 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 muscle cell transplantation. Among all these non-satellite myogenic stalk cells, human mesoangioblasts, human being myogenic-endothelial cells and homo muscle–derived CD133+ accept shown myogenic potentials in vitro and in vivo (Sampaolesi et al. 2006; Zheng et al. 2007; Meng et al. 2022). The utilize of such myogenic progenitors cells for improving musculus healing may become an interesting therapeutic alternative (Tedesco and Cossu 2022; Tedesco et al. 2010; Chen et al. 2022). A beginning stage I/IIa clinical trial has recently demonstrated that intra arterial injections of homo mesoangioblasts are safe but display only very limited clinical efficacy in Duchenne patients (Cossu et al. 2022).

Scaffolds

Myogenic forerunner cell survival and migration is greatly increased by 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 musculus regeneration (Borselli et al. 2022). Ideally, using an appropriate extracellular matrix (ECM) composition and stiffness, scaffolds should best replicate the in vivo milieu and mechanical microenvironment (Gilbert et al. 2010) (Engler et al. 2006). A combination of stem cells, biomaterial-based scaffolds and growth factors may provide a therapeutic pick to improve regeneration of injured skeletal muscles (Jeon and Elisseeff 2022).

Anti-fibrotic therapy

TGF-β1 is expressed at high levels and plays an of import role in the fibrotic cascade that occurs after the onset of muscle injury (Bernasconi et al. 1995; Li et al. 2004). Therefore, neutralization of TGF-β1 expression in injured skeletal musculus should inhibit the formation of scar tissue. Indeed, the employ of anti-fibrotic agents (ie decorin, relaxin, antibody against TGF-β1…) that inactivate TGF-β1 signaling pathways reduces muscle fibrosis and, consequently, meliorate muscle healing, leading to a well-nigh complete recovery of lacerated muscle (Fukushima et al. 2001; Li et al. 2007). Losartan, an angiotensin II receptor antagonist, neutralize the outcome of TGF-β1 and reduce fibrosis, making information technology the treatment of choice, since information technology already has FDA approval to be used clinically (Bedair et al. 2008; Park et al. 2022; Terada et al. 2022). Suramin, also canonical by the FDA, blocks TGF-β1 pathway and reduces muscle fibrosis in experimental model (Chan et al. 2003; Taniguti et al. 2022).

Mechanical stimulation

Mechanical stimulation may offer a simple and effective approach to enhance skeletal musculus regeneration. Stretch activation, mechanical conditioning but also massage therapy or concrete manipulation of injured skeletal muscles have shown multiple do good effects on musculus biological science and function in vitro and in vivo (Tatsumi et al. 2001);(Best et al. 2022) (Crane et al. 2022; Kumar et al. 2002; Gilbert et al. 2010; Powell et al. 2002). Recently, Cezar and colleagues demonstrates that mechanical forces are equally of import biological regulators as chemicals and genes, and underlines the immense potential of developing mechano-therapies to treat musculus damage (Cezar et al. 2022). A recent study also demonstrated that a treatment based on ultrasound-guided intra-tissue percutaneous electrolysis (EPI technique) enhances the treatment of muscle injuries (Abat et al. 2022). Altogether, these results propose that mechanical stimulation should exist 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 problems in traumatology. Despite their clinical importance, the optimal rehabilitation strategies for treating these injuries are non well defined. Later on a trauma, skeletal muscles have the capacity to regenerate and repair in a complex and well-coordinated response. This process required the presence of diverse prison cell populations, up and down-regulation of diverse gene 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 animal models. A better understanding of the cellular and molecular pathways also as a improve definition of the interactions (prison cell-cell and cell-matrix) that are essential for constructive muscle regeneration, should contribute to the development of new therapies in humans. In this direction, a recent newspaper 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. 2022).

Abridgement

CTGF, connective tissue growth factor; FGF, fibroblast growth factor; HGF, hepatocyte growth cistron; IGF-I, insulin similar growth gene-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 factor

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 approved the concluding manuscript.

Contributor Information

Thomas Laumonier, Phone: +41 22 3795393, Electronic mail: hc.eginu@reinomual.samoht.

Jacques Menetrey, Email: hc.eguch@yertenem.seuqcaj.

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