Duchenne On the other hand, upon chronic exercises, the degeneration and inflammatory infiltration of the gastrocnemius muscle, but not the diaphragm, turned to be increased in Nrf2tKOmdx in comparison to mdx mice. m. [Reproduced, with permission, from reference (244)]. skeletal muscle subjected to prolonged eccentric training. However, for large volumes of muscle loss, this regeneration needs interventional support. The ear-, liest studies of satellite cell activation in response to damage, showed that injury caused the release of mitogens from the, muscles themselves. 177. Synthesis C5a that is generated by C5 cleavage can increase histamine release by, mast cells, which drives edema and further inﬂammation that can promote muscle damage. For that, the following objectives were (i) to comprehensively assess the physiological mechanisms and recovery pattern of neuromuscular fatigue of the hamstring muscle group following an intermittent sprint (IS) intervention; (ii) to investigate inter-individual differences in skeletal muscle repair/recovery after an artificial wounding (scratch) assay using of primary human skeletal muscle cells in vitro; (iii) to ascertain whether multiple genetic variations, which are linked to varying tissues, forming a polygenic profile could distinguish between high and low responders following muscle damage in vivo and in vitro; and (iv) to assess whether a genetic profile is linked with the response to both EIMD and chronic resistance exercise. RB6-8C5 is a monoclonal antibody that binds, trophils and monocytes; binding RB6-8C5 would selectively, opsonize neutrophils and monocytes, leading to their selec-, depleted by generation of a mouse strain that expressed a, transgene encoding the diptheria toxin (DPT) receptor gene, with DPT before muscle injury (6). However, cumulation of extracellular marker dyes into injured muscle, ﬁbers and the increased concentration of cytosolic proteins, from muscle in the extracellular space is progressive for days, following increased muscle loading or after the application, of eccentric contractions (40, 106, 114). Activation of neutrophils by IFN, production and release of MPO, which can also promote cytotoxicity and muscle damage. 2002; Jarvinen et al. Muscle dam-, age during IR was also reduced by blocking the function of, adhesion molecules that mediate neutrophils adhesion to the, vascular endothelium, which is a prerequisite for their extrav, sation (diapedesis). The treadmill running conditions, also caused increased inﬂux of extracellular tracer dye, sug-, gesting that the loss of cytosolic FGF2 resulted from leakage, through exercise-induced injuries to the cell membrane. For example, the large, rapid efﬂux of c, tosolic proteins such as creatine kinase that occurs following, treatment of muscle with a calcium ionophore is effectively, blocked by inhibiting phospholipase activity with chlorpro-, mazine or inhibiting lipoxygenases with NDGA (60) and the, cle membrane lysis and microscopically discernible holes in, muscle cell membranes (89). This ﬁnding suggests that hy-, droxyl radicals derived from superoxide are more likely to, be the damaging reactant, although disruptions in superoxide, production or metabolism could have downstream ef. Other investigations raise questions concerning the im-, portance of phagocytosis in the process of muscle repair and, regeneration. Arginase acts as an alternative pathway of L-arginine metabolism, proliferation and differentiation of myoblasts derived from adult mouse. YM. Many feaures in the injury-repair-. injury following ischemia and reperfusion. Null mutation of either CCR2 or CCL2 pro-, duced tremendous reductions in the numbers of macrophages. These adult stem cells are normally in a quiescent state but, due to environmental cues, such as muscle injury, exercise, eccentric strength as other triggers, they become activated (Dreyer et al., 2006;Fu et al., 2015;Snijders et al., 2015). Chanoine C. Expression and neural control of myogenic regulatory fac-. in MPC proliferation, without affecting fusion rates (108), but can also inﬂuence the survival of myotubes by blocking, apoptosis can be induced, leading to loss of muscle, but IFN, to stimulate muscle repair and regeneration by increasing the. by neutrophils and the complement membrane attack complex. F, Saillant G, Butler-Browne GS, Mouly V. Skeletal muscle regenera-, VS, Slocum GR, Bain JL, Sedlak FR. 15). The synthesis and, release of signaling molecules that are activated by muscle, ﬁbers subjected to membrane damage can induce the activa-, tion and attraction of a diverse population of cells that promote, jury, the sequence of muscle injury-repair, to full functional recovery with days to weeks of the initial, Despite the necessity of successful repair of damaged muscle, cell membranes for the re-establishment of muscle homeosta-, been stimulated by the discovery that some inherited, pro-, gressive muscular dystrophies that include limb girdle mus-, cular dystrophy 2B (LGMD2B) and Miyoshi myopathy can, be caused by null mutation of a gene that encodes a pro-, a protein called dysferlin (138), is located in the cytoplasm, and at the cell surface of muscle ﬁbers and dysferlin-null mice, show an increased occurrence of muscle ﬁbers that contain el-, evated concentrations of tracer molecules normally restricted, crease membrane damage in dysferlin-null mice (11), which, suggests that the increased membrane damage in dysferlin-, deﬁcient mice does not reﬂect increased susceptibility of the, membranes to mechanical damage. Nevertheless, transcriptional ablation of Nrf2 in mdx mice did not significantly aggravate the most deleterious, pathological hallmarks of DMD related to degeneration, inflammation, fibrotic scar formation, angiogenesis, and the number and proliferation of satellite cells in non-exercised conditions. Many key studies concerning both aerobic. dystrophin (B) A longitudinal section of a strained muscle preserved imme-, diately following injury showing the distal MTJ region of muscle ﬁbers. The early stages of muscle repair following injury are characterized by a contemporaneous invasion of neutrophils (PMN) and M1 macrophages with the activation of expression of transcription factors associated with the proliferative stage of myogenesis (e.g., MyoD and Myf5). Now, here are the big do’s you want to do as you approach proper muscle recovery. HHS 12). However, of creatine kinase from rat soleus muscles experiencing injury, caused by eccentric contractions was greater at higher strain, rates (265), which may indicate that cell membrane damage, is strain rate dependent, while myoﬁbrillar damage is strain, Some of the apparent discrepancy between the identiﬁca-, tion of the mechanical parameters that primarily determine the, magnitude of injury in these investigations may be explained, by differences in the muscles tested and the treatment proto-, cols. leased or activated, an innate immune response is initiated, satellite cells are activated and muscle repair and regenera-, pathogenic sequence is directly or indirectly attributable to, Empirical evidence provides strong support for the conclusion, that membrane damage in dystrophin-deﬁcient muscle ﬁbers, can be caused by mechanical stresses placed on the muscle, cell membrane and that this is a primary defect in the dis-, ease (189). Bone. Genetic studies first identified the mechanosensory signaling network that connects the structural elements of muscle and, more recently, have identified repair elements of muscle. fibers. Evidence is also presented to show that the myogenic program that is activated by acute muscle injury and the inflammatory process that follows are highly coordinated, with myeloid cells playing a central role in modulating repair and regeneration. cell cultures increases proliferation of the unstimulated cells, and treating stimulated cells with neutralizing antibodies to, Myogenic cell migrations to sites of repair, Severe muscle injuries that are caused by crush, toxin expo-, sure, burns, or freezing can deplete satellite cells at the injury, site, in addition to causing necrosis of muscle ﬁbers at the, site. The role of Nrf2 in the pathophysiology of skeletal muscles has been evaluated in different experimental models, however, due to inconsistent data, we aimed to investigate how Nrf2 transcriptional deficiency (Nrf2tKO) affects muscle functions both in an acute and chronic injury. CCR2-/- mice during impaired skeletal muscle regeneration. Xu H, Lee CW, Wang YF, Huang S, Shin LY, Wang YH, Wan Z, Zhu X, Yung PSH, Lee OK. Front Bioeng Biotechnol. Loss of desmin, also reduces muscle ﬁber stiffness during eccentric contrac-, tions (208) and can reduce the susceptibility of muscles to, injury during eccentric contractions (208). Desmin, the most prevalent intermediate ﬁlament protein in, skeletal muscle, links Z-disks to one another in series, in, parallel and to the cell membrane at costameres and at the, MTJ (86, 191, 239). However, in injured mouse muscle, Xin expression is up-regulated and observed throughout skeletal muscle fibers and within satellite cells. Some of the loss of desmin from sections, of ﬁbers could reﬂect mechanical damage of the desmin ﬁla-, ments, leading to their retraction away from the desmin-free, (A) The muscle on the left was photographed immediately after the. The magnitude of unregulated, inﬂux of cytosolic calcium corresponds to the magnitude of, subsequent leakage of cytosolic proteins into the extracellular, space (68), suggesting that much of the increase in membrane, damage may be secondary to process that are regulated by, calcium. catalytic the immune system during muscle regeneration. Because much of the myeloid-cell-mediated damage to, activation promotes the expression of iNOS in macrophages, thereby increasing the production, of NO to levels that can be cytotoxic. These functions of IFNγ appear to be most important during the Th2 inflammatory response while muscle repair and regeneration proceed. These, ﬁndings indicated an important role for macrophages in those, and differentiation during reloading were disrupted. Null mutation of myeloperoxidase (MPO), which catalyzes, the formation of hypocholorous acid from superoxide-derived, hydrogen peroxide, prevented most of the muscle membrane, lysis that occurred in reloaded soleus muscles, icity by neutrophils. Thus, the elevated lev, that accompany acute (35) and chronic (258) muscle injuries, have the potential to amplify the innate immune response, and, potentially to exacerbate muscle damage that occurs during, ﬂuence repair and regeneration following injury that may be, beneﬁcial to the repair process (Fig. The in-, complete understanding of the speciﬁc mechanical parame-, ters that cause muscle damage during eccentric contractions is, surprising. muscle and transverse passive mechanical properties of muscle (22), suggesting a functional role for desmin in integrating the pas-, sive mechanical properties of muscle cells. Manipulating the timing of Stat3 signals affects this balance. In conclusion, the microbiopsy technique allows more focused muscle research in young CP patients. nNOS For example, why does the relativ, strain, strain rate, force, and work in the occurrence of muscle, injury during eccentric contractions differ between inv, tions? Macrophages and skeletal muscle regener-. tein Animal studies have shown that following aseptic myotrauma, antioxidant and/or anti-inflammatory supplementation leads to an improved recovery and skeletal muscle regeneration through enhanced SCs kinetics, suggesting a redox-dependent molecular mechanism. Can a, better understanding of the speciﬁc mechanical parameters, that cause myoﬁbril damage aid in the design of exercise or. timelapse analysis of muscle satellite cell motility. Satellite cells are tissue resident muscle stem cells required for postnatal skeletal muscle growth and repair through replacement of damaged myofibers. the body leaves them further vulnerable to acute injuries by exposure to extreme temperatures, contusions, lacerations or toxins. helix family (bHLH), that includes MyoD, myogenin, Myf4, and Myf5 (reviewed by references 128, 139). Furthermore, assays using permeabilized ﬁbers indicate that a, signiﬁcant portion of the damage that is reﬂected in deﬁcits in, force production results from direct mechanical disruption of, What are the sites of muscle injury during, Muscle injuries during eccentric contractions that lead to com-, plete muscle tears occur primarily at or near myotendinous, junctions (MTJs), which are specialized, mechanical junc-, tions at which contractile forces are transmitted from the mus-, cle ﬁber to the extracellular matrix at the ends of muscle ﬁbers, ure occurs at the MTJ is inﬂuenced by the activation state of, the muscle, and perhaps varies with the muscle experiencing, loading or with the species of animal used for assay. Therefore, the overall aim of this PhD thesis was to investigate the physiological and genetic factors underpinning the response to muscle damaging exercise. Arrows marked “B” represent events that occur during the early, differentiation stage of regeneration. demonstrating differentiation through MyoD protein destabilization. Furthermore, the relatively superﬁcial location of many muscles in. cles with the surface membrane of muscle cells. 7). The resulting replacement of muscle by fatty and fibrous tissue leaves muscle increasingly weak and nonfunctional. [Adapted and modiﬁed, with permission, from reference (93)]. Lecture announcement for a presentation by Professor D.R. Actuellement, de nombreuses stratégies anti-fibrotiques se développent mais aucune n’a encore été capable de réduire une fibrose pré-existante. by causing excessive hydrolysis of membrane phospholipids, leading to further membrane defects. In this article, the, process of muscle injury, repair and regeneration that occurs in muscular dystrophy is used as, an example of chronic muscle injury, to highlight similarities and differences between the injury. Previous research reported altered muscle properties, such as reduced volume and satellite cell (SC) numbers and hypertrophic extracellular matrix compared to typically developing (TD) children (>10 years). Hence, in general, we demonstrated that the deficiency of Nrf2 transcriptional activity has no profound impact on muscle pathology in various models of muscle injury. Mi-, crovascular effects of complement blockade with soluble recombinant. (258), which is characterized by elevated expression of IL-4, CD206, and arginase (84, 146). Nous avons caractérisé les populations cellulaires non-myogéniques (CD56-) de muscles contrôles et fibrotiques et montré que les cellules CD56- de muscles fibrotiques ont un phénotype différent des cellules de muscles contrôles (capacité proliférative, sensibilité au TGFβ, sécrétion, impact sur la fusion et la régénération). Experimental evidence for the protective ef, against inﬂammation of muscle during IR was demonstrated, in rats that received systemic administration of a NOS in-, NO production (75). regeneration, in mice injected with Bothrops asper snake venom. How muscle recovery takes place. domain Muscle has, been a “pioneering” tissue for understanding development and, how transcription factors function to regulate tissue-speciﬁc, gene expression. Several observations supported early expectations that a, signiﬁcant proportion of muscle ﬁber damage, especially mus-, cle membrane damage, may be attributable to the cytolytic, activities of inﬂammatory cells. The mean number of migrating MPCs, and the mean number of MPCs in a proliferation assay were, increased by PDGF-BB, but not PDGF-AA (205). In this latter model, cells. Muscle wasting and impaired muscle regen-. teins reﬂective of later stages of muscle differentiation (152). Bar, separations (S) occurred in the connective tissue near the MTJs in unstimulated muscles strained to failure. Accumulating evidence suggests that phagocytosis of, debris by myeloid cells may provide a negativ, tenuates Th1 activation, and thereby contributes to transition. muscle functional restoration after injury. eCollection 2020. and cardiac protective effects in myocardial ischemia and reperfusion. Although this system provides an effective mechanism for muscle repair and regeneration following acute injury, it is dysregulated in chronic injuries. muscular dystrophy and 4 cases of Becker muscular dystrophy. Other muscle damage measures also showed a correlation with severity [Xin actin-binding repeat-containing 2 (rs = -0.7108, P = 0.0006) and collagen (rs = 0.4683, P = 0.0783)]. 11 and 12). expected to reduce myeloid cell damage to muscle during IR. Furthermore, the extent to which the re-, newal capacity of satellite cells is inﬂuenced by exogenous, sence of other cell types, does the experimental manipulation, or chemokines affect the ﬁnal extent of muscle regeneration, thermore, little is known of the complex interactions that may, that commonly accompanies intense muscle use or muscle in-, jury and the changes in patterns of gene expression in satellite, tions of cytokines that inﬂuence muscle injury, regeneration is needed. clearing tissue debris in preparation for muscle regeneration, tial component of muscle repair and regeneration following, tance of phagocytosis in muscle regeneration may reﬂect dif-, ferences in the injury model used, the method of reducing, phagocytic cell populations, and the assays chosen to assess, repair and regeneration. The early-invading, proinﬂammatory M1 macrophages remove debris caused by injury and express Th1 cytokines. This positive feedback would tend to retain, satellite cells in the proliferative stage if the Th1 inﬂamma-, tory response were perpetuated. Thus, the main goal of this study is to test whether muscle homing of systemically transplanted ADSC can be enhanced by employing muscle-specific chemotactic signals originating from CMD-affected muscle tissue. tion factors coincided with the slowing of cell proliferation, and entry into the early differentiation stage of myogene-, sis (44, 280). Muscle membrane lesions or muscle stretching increases the calcium, ion entry into muscle, producing an increase in nNOS activation. Epub 2020 Aug 5. The subsequent invasion by anti-inflammatory, M2 macrophages promotes tissue repair and attenuates inflammation. Healthy skeletal muscle has a high degree of birefringence, caused by the regular arrangement of myofibrils. The crucial importance of macrophages during muscle repair has recently received a lot of attention. Macrophages are professional phagocytes that secure host defense. Methods: A total of 33 rats were divided randomly into control (n = 3), mild contusion (n = 15), and severe contusion (n = 15) groups; the contusion groups were further divided into five subgroups (1, 3, 24, 48, and 168 h post-injury; n = 3 per subgroup). F, macrophage invasion in toxin-injected muscles was signiﬁ-, cantly reduced by null mutation of CCR2, although neutrophil, the lesion site was slowed in CCR2 null mice (175), so that, part of the regenerative defect may be attributable, cient blood supply. The elevated production of proinﬂamma-, tory cytokines can then further promote activation of M1, macrophages. bearing (the unloading/reloading model). of injury and repair mechanisms in other tissues. GS. Evidence shows that muscle injuries that are caused by eccentric contractions result from direct mechanical damage to myofibrils. Background: Muscle trauma frequently occurs in daily life. in mouse embryonic limb myogenic cells in vitro. We consider the evidence that striated muscle contains filaments that have average diameters intermediate between those of actin and myosin and that are neither thick (myosin) filaments nor thin (actin) filaments. membrane, leading to defects in plasma membrane repair. Sub-, sequent work showed that FGF2 released from mechanically, loaded muscle cells could promote myogenic cell prolifera-, tion. Some of the activated cells then exit from the cell cycle and return to their niche as quiescent satellite cells to renew and maintain the satellite cell population. Healthy, v, tal muscle can routinely generate stresses that exceed 0.3 MPa, at frequencies that exceed 10 Hz without experiencing injury, creased several-fold when external loads are applied while a, muscle is actively generating force under conditions called, lengthening contractions or eccentric contractions. HGF can then bind its receptor c-met that is present on the surface of quiescent, satellite cells to induce their activation, proliferation, and chemotaxis. These were compared with 6 control biopsies which were morphologically normal. To this end, new methods for studying muscle samples of young children, valid to delineate the features and to elucidate the regenerative potential of muscle tissue, are necessary. Similar reductions, inﬂammation was reduced by treating with glucocorticoids, (272), or null mutation of MMPs that can activate the in-, ﬂammatory response (133) or by treating with metallopro-. These functions of TNF, to increase their proliferation and suppress their differentiation. promote later stages of muscle repair and regeneration (Fig. The products of C3 cleavage, C3a and C3b, can contribute to muscle inﬂammation and injury, through multiple effects. are primarily neutrophils and iNOS-expressing, phagocytic. However, expressed by endothelial cells, macrophages, and dendritic, cells in the injured muscle (264), so that part of the CCL2, effect on regeneration could be mediated by those other cell, Other ﬁndings show that signaling through CCL2/CCR2, in injured muscle has direct effects on the inﬂammatory, process that may underlie the defects in regeneration that, are caused by ablating this signaling pathway. Although mesenchymal stem cells (MSCs) have been shown as a novel approach in tissue regeneration, the therapeutic potential of MSCs mediated by the interaction between MSC-derived paracrine mediators and Mφs remains elusive. C3b can amplify muscle inﬂammation and damage by participat-, ing in the cleavage of C5. Ho, clin D1 (8, 90, 97), which can increase cell proliferation and, crease degradation of MyoD protein (123), which would neg-, in the proliferative stage of myogenesis. Taken together, these data demonstrate Xin as a useful biomarker of muscle damage in healthy individuals and in patients with myopathy. Criswell DS. On one hand, NO, can cause cell membrane damage, either through direct ac-, tions as a free radical, or through its subsequent conversion, to another free radical, such as peroxynitrite (ONOO. The acute muscle damage was induced in mice of two genotypes – WT and Nrf2tKO mice by cardiotoxin (CTX) injection. The nuclear factor erythroid 2-related factor 2 (Nrf2) is considered as a master cytoprotective factor regulating the expression of genes encoding anti-oxidant, anti-inflammatory, and detoxifying proteins. II. Elevations in cytosolic calcium also in-, crease membrane repair by enabling dysferlin and annexins, to bind one another and to bind membrane phospholipids as, part of the membrane-resealing process. Upon, completion of terminal differentiation, the central nuclei migrate to the surface of the muscle. Early studies, showed that the onset and severity of muscle damage dur. 2020 Aug 4;7(3):86. doi: 10.3390/bioengineering7030086. Increased oxidative stress may be the most important, among the many nonphysiological stresses applied to satellite, conditions place cells in 5% carbon dioxide and ambient pO. early stages of muscle repair may result from activation of, is retained in the cytoplasm in an inactive form when it is, bound to endogenous inhibitors. This review focused on the elucidation of paracrine crosstalk between MSCs and Mφs during musculoskeletal diseases and injury. reloading-induced changes in rat soleus muscle. Epub 2013 Jan 18. GLGF 3.3. We have observed slightly increased muscle damage in Nrf2tKO mice after CTX injection. Although, these ﬁndings show important roles for macrophages that are, present in 2 to 4 days of reloaded muscle in promoting mus-, by M2 macrophages because the depletion protocol may also. Defective membrane repair in dysferlin-. ameliorates muscular dystrophy in mdx mice. associated with injury to skeletal muscle ﬁbers. These polygenic profiles may be used to anticipate an individual’s response/adaptation to EIMD and to chronic resistance exercise, thus enabling resistance exercise to be prescribed on a personalised level to improve muscle health and function. muscle, reaching a peak at 5-day postinjury, and then de-, clining (35). intact human polymorphonuclear leukocytes. HGF is expressed by mesenchymal, cells (224) and can be stored in the extracellular matrix, in-. Dans le muscle squelettique c’est une caractéristique pathologique commune à plusieurs dystrophies dont la dystrophie musculaire oculopharyngée et la dystrophie musculaire de Duchenne (DMD). Because of the, large number of essential physiological functions served by, muscle, insufﬁcient repair or regeneration of muscle can af-, fect the viability of the organism. Immunohistochemical analysis of, desmin distribution in cross-sections of rabbit muscle shows, that cyclic application of eccentric contractions cause a loss of, anti-desmin labeling in a small but signiﬁcant portion of mus-, cle ﬁbers (71, 137). Compr Physiol 1:2029-2062, 2011. Furthermore, ad-, ministration of an antibody that blocks the respiratory burst, and degranulation of neutrophils prior to eccentric contrac-, tions caused great reductions in morphologically discernible, damage to muscle (26). Other investigators ha, shown that the absolute twitch force and tetanic force pro-, ated by healthy muscle, although much of the difference was, whole animal function also reveal the danger of concluding, lack of muscle injury when no difference in a single metric, of injury is identiﬁed. is metabolites that drive the proliferation of cells, including ﬁbroblasts. In all cases necrotic fibres labelled intensely with C9 and C8 but intensities varied with the different monoclonal antibodies. Kobzik L, Zhang M, Hechtman HB, Moore FD Jr, Carroll MC. 2010 Feb;81(1):11-20. doi: 10.1111/j.1740-0929.2009.00712.x. C5a, can also increase the production of potentially cytotoxic free radicals by neutrophils and elevate, the expression of Th1 cytokines, which could further elevate inﬂammation and inﬂammatory cell-, mediated damage to muscle cells. To withstand the rigors of contraction, muscle fibers have specialized protein complexes that buffer against mechanical stress and a multifaceted repair system that is rapidly activated after injury. Eccentric, contractions are the most common cause of acute muscle in-, important in determining muscle injury during, Although exercise-induced muscle injuries most typically oc-. In particular, vated expression of arginase in M2 macrophages in, brosis in these chronically injured muscles. RH Jr. Dysferlin interacts with annexins A1 and A2 and medi-. MMP-mediated, cleavage of HSP core protein permits the release of HGF and FGF2 from their bound, inactive state, to become active. Physiological role of tumor necrosis factor alpha, tribution of cell membrane probes following contraction-induced injury. is necessary for terminal differentiation of embryonic limb muscle. The uncertainty of whether replica-, tive senescence of satellite cells that has been described, current knowledge. Instead, the suppressed expression of many, the promoter of the transcriptional repressor YY1, leading, to increased expression of YY1, which then represses the, expression of multiple genes that are upregulated in late dif-, long after myogenic cells have exited the proliferativ, myogenesis and entered the early-to-terminal stages of differ-, entiation, suggesting an additional regulatory role for TNF, in later stages of muscle regeneration (Fig. function is tightly regulated, and its activation occurs, -mediated, intracellular processes or produced by, activation in contributing to muscle membrane injury, is greatly reduced by the presence of exogenous su-, gene in mice that were subjected to hindlimb un-, -arginine, the substrate for NOS that can increase, Simpliﬁed schematic representing some of the steps of the complement cascade that, Schematic representation of the cycle of satellite cell activation, proliferation, and, also increases HGF release into the culture, Schematic representation of a potential mechanism through which muscle injury could, Diagrammatic representation of the temporal relationship between, Diagram of alternative fates of macrophages activated to the M1 phe-, is a prototypical Th1 cytokine and powerful acti-, is generally viewed as a product of only natural, can serve an autocrine role driving M1 macrophage acti-, may also have direct effects on muscle cells to in-, , and endotoxin (287) suggesting that IFN, in muscle following acute injury would be expected, Simpliﬁed summary diagram of the competing roles played by IFN, can be expressed and secreted by M1 macrophages, further driving monocytes to, appear to be most important during the Th1 inﬂammatory response. thase complexed with dystrophin and absent from skeletal muscle sar-, TM. Hence birefringence is usable as a source of image contrast for, Skeletal muscle regenerates efficiently following injuries and diseases. Localization of the DMDL gene-encoded dystrophin-. The potential cytotoxicity of superoxide, bly contribute to muscle damage through this process.
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