ライフサイエンスコーパス: muscle regeneration

1 ty to resume proliferation and contribute to muscle regeneration.

2 ned whether lipin1 contributes to regulating muscle regeneration.

3 f Rbfox1 in satellite cells does not disrupt muscle regeneration.

4 and molecular mechanisms underlying skeletal muscle regeneration.

5 tem cell, or satellite cell, is required for muscle regeneration.

6 FGFR4 is involved in myogenesis and muscle regeneration.

7 AT2R antagonist PD123319 during CTX-induced muscle regeneration.

8 at Nrf2-deficient mice therefore have poorer muscle regeneration.

9 s, and recruited macrophages during skeletal muscle regeneration.

10 f macrophage/monocyte subsets is critical to muscle regeneration.

11 ndent transcriptome associated with skeletal muscle regeneration.

12 recovery of hindlimb perfusion and superior muscle regeneration.

13 e in regulating myoblast differentiation and muscle regeneration.

14 in satellite cells during acute and chronic muscle regeneration.

15 oves the efficacy of the transplantation and muscle regeneration.

16 orts have not observed ECM-mediated skeletal muscle regeneration.

17 oD expression during embryogenesis and adult muscle regeneration.

18 irects cell activities essential for cardiac muscle regeneration.

19 HIF-1alpha is required for adequate skeletal muscle regeneration.

20 siently during injury-induced adult skeletal muscle regeneration.

21 e, and that S1P biosynthesis is required for muscle regeneration.

22 m cell dynamics during homeostatic aging and muscle regeneration.

23 c deletion of MASTR in mice impairs skeletal muscle regeneration.

24 or muscle growth and maintenance and one for muscle regeneration.

25 pathway during myoblast differentiation and muscle regeneration.

26 This promotes efficient muscle regeneration.

27 other and with damaged myofibers to promote muscle regeneration.

28 , promote muscle degeneration and failure of muscle regeneration.

29 skeletal muscle, identifying a novel role in muscle regeneration.

30 the noncanonical Wnt pathway during skeletal muscle regeneration.

31 ned satellite cell proliferation and impeded muscle regeneration.

32 suggesting a mechanism by which A20 promotes muscle regeneration.

33 t in integrin-beta3 function could stimulate muscle regeneration.

34 ignaling to induce SC differentiation during muscle regeneration.

35 of Trpc1 in myoblast differentiation and in muscle regeneration.

36 regulatory network underlying the process of muscle regeneration.

37 critical for designing therapy for skeletal muscle regeneration.

38 complex, as a pivotal regulator of skeletal muscle regeneration.

39 b ischemia promoted significant vascular and muscle regeneration.

40 ed role of intramuscular adipose in skeletal muscle regeneration.

41 they are essential for acute injury-induced muscle regeneration.

42 n-like growth factor-1 (IGF-1), and impaired muscle regeneration.

43 g neural cell adhesion molecule, a marker of muscle regeneration.

44 for Abcg2 in positively regulating skeletal muscle regeneration.

45 s to reduce fibrosis and facilitate skeletal muscle regeneration.

46 ribute significantly to efficient, effective muscle regeneration.

47 , fiber-type determination, hypertrophy, and muscle regeneration.

48 lite cells are the only stem cell source for muscle regeneration.

49 efficient activation of mTORC1 and promotes muscle regeneration.

50 igrate into damaged muscle and for efficient muscle regeneration.

51 f-perpetuating process leading to incomplete muscle regeneration.

52 ecause augmented IGF-1 signaling can improve muscle regeneration.

53 out were used to examine how the HFD changes muscle regeneration.

54 d found impaired satellite cell function and muscle regeneration.

55 and produce a high level of IGF-I to promote muscle regeneration.

56 r apex and contribute prominently to cardiac muscle regeneration.

57 and their cellular functions with respect to muscle regeneration.

58 muscle injury model, lack of MKP-1 impaired muscle regeneration.

59 ayed a high self-renewal rate, which impairs muscle regeneration.

60 tronic enhancer activity, leading to lowered muscle regeneration.

61 mobilizes stem cells and restores youth-like muscle regeneration.

62 r of SC and MP amplification during skeletal muscle regeneration.

63 AMPKalpha1 in satellite cell activation and muscle regeneration.

64 d4 in aged SCs did not promote aged skeletal muscle regeneration.

65 their deficits in Treg cell accumulation and muscle regeneration.

66 uring SC differentiation, and it potentiates muscle regeneration.

67 roves the myopathy phenotype is by promoting muscle regeneration.

68 peded satellite cell activation and impaired muscle regeneration.

69 peutic potential to improve in situ skeletal muscle regeneration.

70 active H3K27 demethylation is necessary for muscle regeneration.

71 Smad4 disruption compromised adult skeletal muscle regeneration.

72 ed by many complications, including impaired muscle regeneration.

73 ll deficit which unexpectedly did not affect muscle regeneration.

74 oRNAs (miR-1 and -206) to further accelerate muscle regeneration.

75 utation also resulted in functional striatal muscle regeneration.

76 r (ALK4) as a mediator of muscle atrophy and muscle regeneration.

77 ich is required for satellite activation and muscle regeneration.

78 ibits cardiomyocyte proliferation and delays muscle regeneration.

79 ifferentiation and reduces the efficiency of muscle regeneration.

80 ces myogenic differentiation and accelerates muscle regeneration.

81 tivation and myogenic differentiation during muscle regeneration.

82 de skeletal muscle and are indispensable for muscle regeneration.

83 f the MEF2A transcription factor in skeletal muscle regeneration.

84 fast oxidative type IIa fibers, and impaired muscle regeneration ability, which are the reverse of wh

85 1(hi) macrophage populations during skeletal muscle regeneration after a sterile damage.

86 her there is any significant contribution to muscle regeneration after acute injury from cells other

87 t the REV-ERB antagonist, SR8278, stimulates muscle regeneration after acute injury.

88 t, there is little or no significant cardiac muscle regeneration after an injury such as acute myocar

89 gene also reduced muscle injury and improved muscle regeneration after cardiotoxin injury, as well as

90 like domain of myospryn displayed attenuated muscle regeneration after cardiotoxin-induced muscle inj

91 f NKX2-5 over-expression, we find defects in muscle regeneration after induced damage, similar to tho

92 Insufficient skeletal muscle regeneration after injury often impedes the heali

93 Muscle regeneration after injury was also impaired in Ba

94 Using a mouse model of skeletal muscle regeneration after injury, we identified hexameth

95 H19-deficient mice display abnormal skeletal muscle regeneration after injury, which is rectified by

96 uency hearing deficits and impaired skeletal muscle regeneration after injury.

97 addition, miR-26a is induced during skeletal muscle regeneration after injury.

98 eveal a role for soluble CD163 in regulating muscle regeneration after ischaemic injury.

99 inhibition of Bhlhe40 or p53 may facilitate muscle regeneration after ischemic injuries.

100 owever, HIF1alpha negatively regulates adult muscle regeneration after ischemic injury, implying that

101 However, muscle regeneration after late (day 4) ablation was simi

102 However, the lack of Anx A1 delayed muscle regeneration after notexin-induced injury.

103 iven mechanical compressions led to enhanced muscle regeneration and a approximately threefold increa

104 idence that satellite cells are required for muscle regeneration and also identify resident fibroblas

105 are medically relevant targets for enhancing muscle regeneration and ameliorating muscle pathology.

106 ion, low resveratrol doses promoted in vitro muscle regeneration and attenuated the impact of ROS, wh

107 toration of glycosylation is associated with muscle regeneration and dependent on the expression of b

108 reviously unknown role of lipin1 in skeletal muscle regeneration and expands our understanding of the

109 In addition, muscle regeneration and growth were greatly slowed by lo

110 in the regulation of satellite cell-mediated muscle regeneration and identify HEXIM1 as a potential t

111 e new insights into the genetic circuitry of muscle regeneration and identify MASTR as a central regu

112 show age-dependent delays in injury-induced muscle regeneration and impaired muscle function.

113 stabilization of the motor nerves results in muscle regeneration and in atrophy especially in the cas

114 tellite cell differentiation during skeletal muscle regeneration and indicate that miR-206 slows prog

115 ificantly from therapies that both stimulate muscle regeneration and inhibit fibrosis.

116 lite cell is the primary cellular source for muscle regeneration and is equipped with the potential t

117 s recognized that epicardium is required for muscle regeneration and itself has high regenerative pot

118 Severe burn injury induces skeletal muscle regeneration and myonuclear apoptosis.

119 e weakness, demyelinating neuropathy, failed muscle regeneration and premature death.

120 to skeletal muscle healing by both promoting muscle regeneration and preventing fibrosis formation.

121 ellular basis of Cripto activity in skeletal muscle regeneration and raise previously undescribed imp

122 , ectopic miR-431 injection greatly improved muscle regeneration and reduced SMAD4 levels.

123 naling in the dKO mice with Y-27632 improved muscle regeneration and reduced the expression of BMPs,

124 the development of potential therapeutics in muscle regeneration and repair.

125 k but not at 6 mo, and it improved diaphragm muscle regeneration and respiratory function at 14 wk bu

126 early embryogenesis, is a novel regulator of muscle regeneration and satellite cell progression towar

127 udy suggests that TWEAK negatively regulates muscle regeneration and that TWEAK is a potential therap

128 elated with sustained inflammation, impaired muscle regeneration and the rapid depletion and senescen

129 e growth factor-1 (IGF1) to directly promote muscle regeneration and the return of muscle function in

130 ances in developing strategies to accelerate muscle regeneration and to slow muscle degeneration in m

131 main display reduced myofiber size, impaired muscle regeneration, and derepression of muscle developm

132 n CKD, including proteolysis, myogenesis and muscle regeneration, and expression of proinflammatory m

133 letal muscle and cardiac pathology, improves muscle regeneration, and extends the lifespan.

134 1 expression is dynamically regulated during muscle regeneration, and mice lacking Sca-1 display incr

135 ficient mice resulted in robust engraftment, muscle regeneration, and proper homing of human PAX7+ sa

136 ling by MEF2A is a requisite step for proper muscle regeneration, and represents an attractive pathwa

137 important role of complement C3a in skeletal muscle regeneration, and suggest that manipulating compl

138 ng changes can also be observed secondary to muscle regeneration, and this possibility must be taken

139 Skeletal muscle fibrosis and impaired muscle regeneration are major contributors to muscle was

140 of specific populations of myeloid cells on muscle regeneration are presented, with an emphasis on h

141 rodents, the potential effects of Ang II on muscle regeneration are unknown.

142 g mainly through the restoration of impaired muscle regeneration, as fibrosis or inflammation was not

143 increased the myopathic lesion size, reduced muscle regeneration, attenuated muscle function, and exa

144 inositol 3,4,5-trisphosphate (PIP(3)) during muscle regeneration because augmented IGF-1 signaling ca

145 to play roles in muscle membrane repair and muscle regeneration, both of which require vesicle-membr

146 nitors (FAPs) that play a supportive role in muscle regeneration but may also cause fibrosis when abe

147 Immune factors are required for muscle regeneration, but chronic inflammation creates a

148 population dedicated to efficacious skeletal muscle regeneration, but their therapeutic utility is cu

149 tment with PGE2 suffices to robustly augment muscle regeneration by either endogenous or transplanted

150 administration of oxytocin rapidly improves muscle regeneration by enhancing aged muscle stem cell a

151 ce, which limits satellite cell function and muscle regeneration by Hoxa9-dependent activation of dev

152 In summary, Mp-derived uPA promotes muscle regeneration by inducing Mp migration, angiogenes

153 Insulin resistance impairs muscle regeneration by preventing myofiber maturation.

154 s of DMD; however, mdx mice display a strong muscle regeneration capacity, while dKO mice exhibit a m

155 in vivo, as USP19(-/-) mice display improved muscle regeneration concomitant with enhanced expression

156 chanism in satellite cell homeostasis during muscle regeneration could help inform research efforts t

157 atellite cells of adult mice led to profound muscle regeneration defects and dramatically reduced lev

158 x7-expressing satellite cells and a profound muscle regeneration deficit that resembles the phenotype

159 te that OVL is beneficial to mdx muscle, and muscle regeneration does not mask the potentially detrim

160 In the muscle biopsy we found evidence of muscle regeneration due to previous necrotic lesions lik

161 that Linc-RAM knockout mice display impaired muscle regeneration due to the differentiation defect of

162 , miR-210 inhibition did not affect skeletal muscle regeneration following cardiotoxin damage.

163 Interestingly, in an in vivo model of muscle regeneration following cardiotoxin injury, ectopi

164 Cobra Venom Factor (CVF) result in impaired muscle regeneration following cardiotoxin-induced injury

165 teady state conditions as well as a delay of muscle regeneration following cardiotoxin-mediated injur

166 strategy to accelerate and enhance skeletal muscle regeneration for the treatment of muscular atroph

167 Signs of muscle regeneration give rise that ischemic muscle damag

168 Much of the focus in muscle regeneration has been placed on the identificatio

169 lls following muscle injury, but its role in muscle regeneration has not been defined.

170 asts, but its potential involvement in adult muscle regeneration has not been explored.

171 to the fundamental pathways that drive heart muscle regeneration have begun to arise as well as a gro

172 , but their potential contributions to adult muscle regeneration have not been systematically explore

173 combined with novel therapies to accelerate muscle regeneration hold promise for future therapy for

174 ults suggest that ERRalpha deficiency during muscle regeneration impairs recovery of mitochondrial en

175 Knockdown of MUNC in vivo impaired murine muscle regeneration, implicating MUNC in primary satelli

176 precursor cell differentiation and improved muscle regeneration in a separate, toxin-induced model o

177 n factor plays an essential role in skeletal muscle regeneration in adult mice.

178 tivation of TAK1 in satellite cells inhibits muscle regeneration in adult mice.

179 f Hoxa9 improves satellite cell function and muscle regeneration in aged mice, whereas overexpression

180 pe littermates, myogenic gene expression and muscle regeneration in cardiotoxin-injured beta3-integri

181 ion of IGF-1, but not PBS, markedly improved muscle regeneration in Ccl2(-/-) mice.

182 muscle to replace IGF-I remarkably improved muscle regeneration in Ccr2(-/-) mice.

183 ng AT2R expression and its potential role in muscle regeneration in chronic diseases, we used a mouse

184 Muscle regeneration in CXCL16-deficient (CXCL16KO) mice

185 molecular switch in the regulation of HO and muscle regeneration in dystrophic skeletal muscle of mic

186 The role of PDGF-BB in muscle regeneration in humans has not been studied.

187 he molecular mechanisms that govern skeletal muscle regeneration in humans.

188 We characterized the time course of skeletal muscle regeneration in lipin1-deficient fld mice after i

189 f MMP-9 significantly augmented the skeletal muscle regeneration in mdx mice.

190 ay gene expression data derived from in-vivo muscle regeneration in mice, both producing biologically

191 icorrelated during cardiotoxin-induced adult muscle regeneration in mice.

192 ates myoblast differentiation in culture and muscle regeneration in mice.

193 We also found that attenuated muscle regeneration in obese mice is rescued by AICAR, a

194 AMPK, but AICAR treatment failed to improve muscle regeneration in obese mice with satellite cell-sp

195 iding a convenient drug target to facilitate muscle regeneration in obese populations.

196 AMPK activity is a major reason for hampered muscle regeneration in obese subjects.

197 ncreased sarcolemmal stability, and promoted muscle regeneration in older mice.

198 on of individual Mef2 genes has no effect on muscle regeneration in response to cardiotoxin injury.

199 vated satellite cell activation and enhanced muscle regeneration in response to CTX injury.

200 te Numb, we determined that, in its absence, muscle regeneration in response to injury was impaired.

201 play decreased IGF2 induction and diminished muscle regeneration in response to injury, indicating th

202 Here, we show that miR-206 promotes skeletal muscle regeneration in response to injury.

203 required in the muscle stem cell lineage for muscle regeneration in response to injury.

204 nuclei observed in muscle fibers suggest for muscle regeneration in these samples.

205 tion of exogenous uPA rescued HGF levels and muscle regeneration in uPA(-/-) mice, and an HGF-blockin

206 ed apoptosis, we report evidence of striated muscle regeneration in vivo in mice by human MiPs.

207 ontrols metabolic remodeling during skeletal muscle regeneration in vivo is unknown.

208 e role of satellite cells and fibroblasts in muscle regeneration in vivo, we created Pax7(CreERT2) an

209 ntial therapeutic target to enhance skeletal muscle regeneration in vivo.

210 oblast differentiation in vitro and skeletal muscle regeneration in vivo.

211 eak inducer of apoptosis (TWEAK) in skeletal muscle regeneration in vivo.

212 sion patterns during myogenesis in vitro and muscle regeneration in vivo.

213 We characterized the time course of skeletal muscle regeneration in wild-type (M-ERRalphaWT) and musc

214 imental model of focal asynchronous bouts of muscle regeneration in wild-type (WT) mice.

215 F-blocking antibody reduced HGF activity and muscle regeneration in wild-type mice.

216 jury AMPK activation was sufficient to delay muscle regeneration in WT mice.

217 crease satellite cell activation and improve muscle regeneration in young mice.

218 nce signaling might impact multiple steps in muscle regeneration, including escape from the niche, di

219 s do not play a crucial role during skeletal muscle regeneration induced by sterile tissue damage.

220 ABSTRACT: Skeletal muscle regeneration is a complex interplay between vario

221 Muscle regeneration is a complex process involving sever

222 tanding the molecular mechanisms of skeletal muscle regeneration is crucial to exploiting this pathwa

223 Muscle regeneration is highly dependent on the ability o

224 Monocyte/macrophage polarization in skeletal muscle regeneration is ill defined.

225 We demonstrate that muscle regeneration is impaired with aging owing in part

226 Skeletal muscle regeneration is mediated by satellite cells (SCs)

227 The effect of complement in muscle regeneration is mediated by the alternative pathw

228 or development and that contrary to mammals, muscle regeneration is normal without functional Pax7 ge

229 eutic use of muscle stem cells for improving muscle regeneration is promising; however, the effect of

230 lite cells are reduced after injury and that muscle regeneration is severely impeded, reminiscent of

231 To define their roles in muscle regeneration, L6E9 cells were used to perform in

232 al of laminin-111 protein therapy to improve muscle regeneration, laminin-111 or phosphate-buffered s

233 hibits satellite cell (SC) proliferation and muscle regeneration, likely contributing to cachexia in

234 Skeletal muscle regeneration mainly depends on satellite cells, a

235 icient satellite cells expanded and improved muscle regeneration more effectively than WT satellite c

236 muscle to suggest its direct involvement in muscle regeneration or angiogenesis.

237 hey can either undergo myogenesis to promote muscle regeneration or differentiate into adipocytes and

238 , which express Abcg2 and may participate in muscle regeneration or may represent a source of satelli

239 l gene inactivation to the tibialis anterior muscle regeneration paradigm, that, unexpectedly, when P

240 Therapies for accelerating muscle regeneration, primarily through inhibition of myo

241 Although the molecular mechanism of muscle regeneration process after an injury has been ext

242 ital imaging for direct visualization of the muscle regeneration process in live mice, we report that

243 a key mediator linking obesity and impaired muscle regeneration, providing a convenient drug target

244 ient muscle was damaged with cardiotoxin and muscle regeneration quantified.

245 ignaling mechanisms governing adult skeletal muscle regeneration remain less understood.

246 alterations that may have a major impact on muscle regeneration remain poorly understood.

247 ish facilitated dynamic live cell imaging of muscle regeneration, repopulation of muscle stem cells w

248 levels, SPL also controls SC recruitment and muscle regeneration, representing a potential therapeuti

249 Muscle regeneration requires the coordinated interaction

250 n adult satellite cells completely abolishes muscle regeneration, resulting in severe muscle destruct

251 Adult skeletal muscle regeneration results from activation, proliferati

252 Blocking Large upregulation during muscle regeneration results in the synthesis of dystrogl

253 n by infiltrating macrophages contributes to muscle regeneration, revealing a novel mechanism of infl

254 Muscle regeneration, sarcolemma integrity and fibrosis w

255 Additionally, burn injury induced skeletal muscle regeneration, satellite cell proliferation and fu

256 is severely impeded, reminiscent of hampered muscle regeneration seen in obese subjects.

257 Analysis of muscle regeneration showed a delay in recovery, probably

258 lexity and can determine the extent to which muscle regeneration succeeds.

259 termine the mechanisms underlying failure of muscle regeneration that is observed in dystrophic muscl

260 We found that AICAR increased skeletal muscle regeneration thereby decreasing the levels of del

261 utant satellite cells are not compromised in muscle regeneration, they can proliferate and reoccupy t

262 t integrin-beta3 plays a fundamental role in muscle regeneration through a regulation of macrophage i

263 ve role in muscular dystrophies by enhancing muscle regeneration through activation of satellite cell

264 rthermore, we demonstrated that UTX mediates muscle regeneration through its H3K27 demethylase activi

265 ng the heart is activated by injury and aids muscle regeneration through paracrine effects and as a m

266 roves satellite cell activation and skeletal muscle regeneration through upregulation of Notch signal

267 ether, our results show laminin-111 restores muscle regeneration to laminin-alpha2-deficient muscle a

268 rentiating into myocytes and contributing to muscle regeneration upon injury.

269 cells that can participate in myogenesis and muscle regeneration upon transplantation.

270 Ang II inhibition of skeletal muscle regeneration via AT1 receptor-dependent suppressi

271 Here we show that Ang II reduced skeletal muscle regeneration via inhibition of satellite cell (SC

272 aling molecule that regulates myogenesis and muscle regeneration via MLX/IGF2/Akt signaling.

273 In vivo, acute cardiotoxin-induced muscle regeneration was enhanced in S1PR3-null mice, wit

274 ressing Abcg2 increased upon injury and that muscle regeneration was impaired in Abcg2-null mice, res

275 pression of myogenic genes was decreased and muscle regeneration was impaired, whereas fibrosis was e

276 Muscle regeneration was induced by cardiotoxin injury, a

277 we used a mouse model of CHF and found that muscle regeneration was markedly reduced and that this w

278 This delay in muscle regeneration was not caused by a slowdown in prol

279 nsistent with this finding, the capacity for muscle regeneration was severely impaired in mice defici

280 In line with in vitro results, muscle regeneration was stimulated, and muscle fiber siz

281 ry and repair, and expression of Mi-2 during muscle regeneration was studied in this model by immunof

282 short-term OVL, which is believed to inhibit muscle regeneration, was not more detrimental to mdx tha

283 the potential involvement of MEF2 factors in muscle regeneration, we conditionally deleted the Mef2a,

284 to develop new strategies that could enhance muscle regeneration, we have developed and performed a h

285 To determine the potential role of AT2R in muscle regeneration, we infused C57BL/6 mice with the AT

286 gnaling in ischemia-induced inflammation and muscle regeneration, we subjected wild-type (WT) and TNF

287 To identify genes involved in muscle regeneration, we used a microarray analysis; ther

288 RP or anti-HMGCR Abs, mechanisms involved in muscle regeneration were also impaired due to a defect o

289 In summary, impairments in muscle regeneration were associated with exaggerated mon

290 early ablation and associated with impaired muscle regeneration were determined by flow cytometry.

291 and central nucleation, indices of skeletal muscle regeneration, were elevated in burn patients (P <

292 hMdm2 construct were unable to contribute to muscle regeneration when grafted into cardiotoxin-injure

293 renew in vitro and contribute extensively to muscle regeneration when subsequently transplanted into

294 n adult satellite cells compromises skeletal muscle regeneration, whereas gain of function of Cripto

295 lation of MyD88 reduces myofiber size during muscle regeneration, whereas its overexpression promotes

296 oxytocin signalling in young animals reduces muscle regeneration, whereas systemic administration of

297 to M2 sequence is observed during postinjury muscle regeneration, which provides an excellent paradig

298 y leads to a profound disruption in skeletal muscle regeneration with an accumulation of SCs within t

299 There was also impaired muscle regeneration with an increase in muscle fibrosis.

300 beta superfamily and a negative regulator of muscle regeneration, with the myostatin antagonist folli