ライフサイエンスコーパス: muscle atrophy

1 be elevated in several settings of skeletal muscle atrophy.

2 patients and mice with inflammation-induced muscle atrophy.

3 ttenuation of inflammation-mediated skeletal muscle atrophy.

4 ey have adaptive mechanisms to reduce disuse muscle atrophy.

5 ysregulated metabolic functions and signs of muscle atrophy.

6 pha) by miR-29b is required for induction of muscle atrophy.

7 aracterized by motor neuron degeneration and muscle atrophy.

8 the treatment of conditions which result in muscle atrophy.

9 onse to this stress may culminate in cardiac muscle atrophy.

10 previously known to play a role in skeletal muscle atrophy.

11 uced insulin resistance, taking into account muscle atrophy.

12 expression of Trim63 (MuRF1), an effector of muscle atrophy.

13 ies, neuromuscular diseases, and age-related muscle atrophy.

14 th MAFbx, a key ubiquitin ligase involved in muscle atrophy.

15 a widely used human model of disuse skeletal muscle atrophy.

16 igated whether hypercapnia leads to skeletal muscle atrophy.

17 /-) mice exposed to high CO2 did not develop muscle atrophy.

18 y distinct from that resulting in GC-related muscle atrophy.

19 We show that HDAC6 is up-regulated during muscle atrophy.

20 nerves, as a process to mitigate neurogenic muscle atrophy.

21 ith ongoing muscle weakness and the onset of muscle atrophy.

22 tic to ameliorate the deleterious effects of muscle atrophy.

23 tosis, microgliosis and ameliorates skeletal muscle atrophy.

24 MCK]-EcSOD) in mice significantly attenuated muscle atrophy.

25 mRNA expression signatures of human skeletal muscle atrophy.

26 ween PGC-1alpha and TWEAK-Fn14 system during muscle atrophy.

27 urons, resulting in progressive weakness and muscle atrophy.

28 rapeutic agent or lead compound for skeletal muscle atrophy.

29 al regulator of denervation-induced skeletal muscle atrophy.

30 idine as a novel small molecule inhibitor of muscle atrophy.

31 1 and Atrogin-1, and progression of skeletal muscle atrophy.

32 echanism through which Dex promotes skeletal muscle atrophy.

33 ation resulting in vacuolation, weakness and muscle atrophy.

34 ific CuZnSOD deletion is sufficient to cause muscle atrophy.

35 erapeutic applications for treating skeletal muscle atrophy.

36 tes to the complicated network that leads to muscle atrophy.

37 tion factors whose activation is critical in muscle atrophy.

38 as a critical target of HDAC4 in neurogenic muscle atrophy.

39 hy, we showed that TRIM32 is dispensable for muscle atrophy.

40 protein (Gadd45a) is a critical mediator of muscle atrophy.

41 r remodeling and a comprehensive program for muscle atrophy.

42 level insights into the etiology of skeletal muscle atrophy.

43 degradation of myofibrillar proteins during muscle atrophy.

44 egeneration of spinal cord motor neurons and muscle atrophy.

45 starvation and muscle disuse cause skeletal muscle atrophy.

46 e and adaptor protein, in starvation-induced muscle atrophy.

47 or its regulatory role in starvation-induced muscle atrophy.

48 of muscle growth in diseases associated with muscle atrophy.

49 a gene, which encodes a critical mediator of muscle atrophy.

50 haracterized by motor neuron loss and severe muscle atrophy.

51 t Bcl3 knockout mice are resistant to disuse muscle atrophy.

52 3 and connexin45 hemichannels, which promote muscle atrophy.

53 actorial regulator of mRNA processing, cause muscle atrophy.

54 r-binding protein beta (C/EBPbeta), mediates muscle atrophy.

55 D receptor (VDR) expression prompts skeletal muscle atrophy.

56 e A(2) (cPLA(2)) derived LOOHs in neurogenic muscle atrophy.

57 etabolite signatures that may be linked with muscle atrophy.

58 ed muscle metabolic alterations and skeletal muscle atrophy.

59 -motor neurons, leading to profound skeletal muscle atrophy.

60 ature death due to loss of motor neurons and muscle atrophy.

61 2)=0.91; P=0.003) and a molecular profile of muscle atrophy.

62 a pharmaceutical target to prevent skeletal muscle atrophy.

63 e shown protection in ground-based models of muscle atrophy.

64 loss of mitochondrial integrity may initiate muscle atrophy.

65 Space Station (ISS) were not protected from muscle atrophy.

66 use these steroids are also known to trigger muscle atrophy.

67 yopathies and age-related/disease-associated muscle atrophies.

68 38.0% NMJs re-innervated; p < 0.02); reduced muscle atrophy (1146 +/- 93.19 um(2) vs 865.2 +/- 48.33

69 Although surgical resection exacerbated muscle atrophy (-7.2%), catabolic changes in protein met

70 hallmark of X-linked myopathy with postural muscle atrophy; a characteristic spongious structure and

71 hether deletion of MuRF1 or MAFbx attenuates muscle atrophy after 2 weeks of treatment with the synth

72 ne regulatory networks that control skeletal muscle atrophy after denervation have been established,

73 t-1 animals also had some protection against muscle atrophy after injury.

74 thing is insufficient, but drawbacks include muscle atrophy, alveolar damage, and reduced mobility.

75 scles from mice exhibited substantially less muscle atrophy, an increase in muscle mass after denerva

76 observed changes in fiber type distribution, muscle atrophy, an increase in satellite cell number, an

77 erspectives on HDAC6 as a valuable marker of muscle atrophy and a potential target for pharmacologica

78 EAA treatment attenuated muscle atrophy and accelerated the return of functional

79 Moreover, both lines displayed denervation muscle atrophy and age-dependent loss of motor neurons t

80 cle disrupting events, eventually leading to muscle atrophy and apoptosis.

81 nAG inhibited dexamethasone-induced skeletal muscle atrophy and atrogene expression through PI3Kbeta-

82 Muscle atrophy and cachexia are common comorbidities amo

83 These signatures of muscle atrophy and cachexia were not influenced by Zip14

84 These defects result in muscle atrophy and compromised swimming behavior, a phen

85 ely, AAV injection resulted in growth delay, muscle atrophy and contracture.

86 sed by SMN deficiency results in progressive muscle atrophy and death in SMA.

87 motor neurons in the spinal cord leading to muscle atrophy and death.

88 eage in skeletal muscle, resulting in severe muscle atrophy and death.

89 triggering the preferential loss of myosin, muscle atrophy and decreased specific force in fast- and

90 6'-sialyllactose ameliorated muscle atrophy and degeneration in symptomatic GNE myopa

91 We evaluated markers of muscle atrophy and denervation, and the myosin/actin rat

92 T3 signaling in the development of diaphragm muscle atrophy and dysfunction during CMV and suggest th

93 -induced protein degradation and rescued the muscle atrophy and dysfunction in a Duchenne muscular dy

94 Skeletal muscle atrophy and endothelial cell dysfunction occur in

95 association (P = .49) between the composite muscle atrophy and fatty infiltration grade (estimate, 0

96 d assessed tendon degeneration and composite muscle atrophy and fatty infiltration using categorical

97 ementally more severe tendon degeneration or muscle atrophy and fatty infiltration).

98 (grade 0 indicates no tendon degeneration or muscle atrophy and fatty infiltration, and higher grades

99 seful both for therapeutic interventions for muscle atrophy and for further investigative areas into

100 Unavoidable periods of disuse lead to muscle atrophy and functional decline.

101 nding the physiological processes underlying muscle atrophy and hypertrophy.

102 a result of an imbalance between drivers of muscle atrophy and hypertrophy.

103 protein level during recovery from skeletal muscle atrophy and hypertrophy.

104 athophysiology with variable combinations of muscle atrophy and impaired contractile capacity.

105 ce is associated with a substantial delay in muscle atrophy and improved motor performance.

106 s expressing SDN had severe, age-accelerated muscle atrophy and increased adiposity, consistent with

107 erized by loss of spinal cord motor neurons, muscle atrophy and infantile death or severe disability.

108 or chronic glucocorticoid exposure leads to muscle atrophy and insulin resistance.

109 oss, fatigue, loss of appetite, and skeletal muscle atrophy and is associated with poor patient progn

110 tein response pathways in starvation-induced muscle atrophy and its regulation through TRAF6.

111 ly impacts key metabolic pathways leading to muscle atrophy and loss of function.

112 resulting in motor neuron (MN) degeneration, muscle atrophy and loss of motor function.

113 ree of autophagy correlates with severity of muscle atrophy and lung function impairment.

114 PLA(2) in vivo mitigates LOOH production and muscle atrophy and maintains individual muscle fiber siz

115 ivin type I receptor (ALK4) as a mediator of muscle atrophy and muscle regeneration.

116 ces changes in type 1 fibers associated with muscle atrophy and muscle weakness in DM1.

117 ted transactivation is often associated with muscle atrophy and other adverse effects of pharmacologi

118 eath of motor neurons leading to spasticity, muscle atrophy and paralysis.

119 Mice with ALI developed profound muscle atrophy and preferential loss of muscle contracti

120 roaches, we showed that AKG rescues skeletal muscle atrophy and protein degradation through a PHD3/AD

121 a mechanism for inhibitory effects of AKG on muscle atrophy and protein degradation.

122 mechanism by which Gadd45a induces skeletal muscle atrophy and provide new insight into the way that

123 14 axis in IBM muscle may induce progressive muscle atrophy and reduce activation and differentiation

124 aracterised ligase termed SMART (Specific of Muscle Atrophy and Regulated by Transcription).

125 Thus, PGE(2) signaling ameliorates muscle atrophy and rejuvenates muscle function, and 15-P

126 mental basis for exosome-mediated therapy of muscle atrophy and renal fibrosis.

127 ss regulation under food deprivation-induced muscle atrophy and TRB3 could be a pharmaceutical target

128 We found SC depletion exacerbated muscle atrophy and type transitions connected to neuromu

129 -AP1 signaling axis essential for neurogenic muscle atrophy and uncover a direct crosstalk between ac

130 cancer cachexia causes profound respiratory muscle atrophy and weakness and ventilatory dysfunction.

131 profound skeletal muscle atrophy; persistent muscle atrophy and weakness are major complications that

132 N-acetylcysteine led to amelioration of the muscle atrophy and weakness in Gne mutant mice.

133 athy, a disease manifesting with progressive muscle atrophy and weakness.

134 related muscle fiber atrophy associated with muscle atrophy and weakness.

135 plained link between hyposialylation and the muscle atrophy and weakness.

136 ism underlying VIDD (i.e., loss of function, muscle atrophy) and identifies RyR1 as a potential targe

137 in capacity for endurance exercise, rates of muscle atrophy, and cardiac function.

138 generation of spinal motor neurons, skeletal muscle atrophy, and debilitating and often fatal motor d

139 (ALS) experience progressive limb weakness, muscle atrophy, and dysphagia, making them vulnerable to

140 of nerve regeneration, neural angiogenesis, muscle atrophy, and functional recovery.

141 racterized by degeneration of motor neurons, muscle atrophy, and progressive weakness.

142 re miR-23a functioned in neuroprotective and muscle atrophy-antagonizing roles.

143 and microglia activation as well as skeletal muscle atrophy are also typical hallmarks of the disease

144 However, the molecular mechanisms of muscle atrophy are complex and not well understood.

145 Mechanisms of muscle atrophy are complex and their understanding might

146 that induce oxidative stress culminating in muscle atrophy are not fully known.

147 for muscle homeostasis is best known during muscle atrophy, as the cullin-1 substrate adaptor atrogi

148 haracterized by motor neuron death, skeletal muscle atrophy, as well as dysfunction and loss of both

149 nce of FoxO activation in the progression of muscle atrophy associated with cachexia.

150 nd expression of mRNAs and proteins encoding muscle atrophy-associated genes for muscle ring finger-1

151 4 (CXCR4) pathway were downregulated only in muscles atrophying because of cancer: stromal cell-deriv

152 stricted to skeletal muscle does not lead to muscle atrophy but does cause muscle weakness in adult m

153 Endurance exercise is effective to attenuate muscle atrophy, but the underlying mechanism has not bee

154 ) have been shown to play a role in skeletal muscle atrophy, but their role is not completely underst

155 egrated stress response that locally induces muscle atrophy, but via secretion of FGF21 acts distally

156 ce of skeletal muscle mass and prevention of muscle atrophy by epigenetic mechanisms via the nNOS/NO

157 imers, we hypothesized that ATF4 may promote muscle atrophy by forming a heterodimer with another bZI

158 d that exosomes containing miR-26a prevented muscle atrophy by inhibiting the transcription factor fo

159 ation may provide a new therapeutic tool for muscle atrophy by short term expansion of the muscle ste

160 y role in regulating Ang II-induced skeletal muscle atrophy by transcriptional control of MuRF1 via c

161 Muscle wasting, or muscle atrophy, can occur with age, injury, and disease;

162 rolonged immobilization (IM) causes skeletal muscle atrophy characterized by mitochondrial deteriorat

163 n have worse muscle function and predominant muscle atrophy compared with those with HF with reduced

164 genic mice increase food deprivation-induced muscle atrophy compared with wild-type (WT) littermates

165 Mini-dystrophin reduction caused muscle atrophy, degeneration and force loss in the TA mu

166 This work provides new insights in skeletal muscle atrophy development and opens interesting perspec

167 In an in vitro model of skeletal muscle atrophy, differentiated C2C12 cells exhibited red

168 Skeletal muscle atrophy due to excessive protein degradation is t

169 mouse model of inflammation-induced skeletal muscle atrophy due to polymicrobial sepsis and cultured

170 ssociation between osteoporosis and skeletal muscle atrophy/dysfunction, the functional relevance of

171 Anti-FHL1 reactivity was predictive for muscle atrophy, dysphagia, pronounced muscle fiber damag

172 al muscle mTORC1 signaling, reduced skeletal muscle atrophy, enhanced recovery from skeletal muscle a

173 shed, myonuclear cell death is activated and muscle atrophy ensues.

174 plasma creatine kinase levels, muscle PDK4, muscle atrophy F-box (MAFbx) and cathepsin-L mRNA expres

175 ly used as a model with which to investigate muscle atrophy following disuse.

176 regulation of multiple genes, including the muscle atrophy gene Trim63.

177 increased the expression of inflammatory and muscle atrophy genes Tnf, Tnfrsf12a, Trim63, and Fbxo32

178 terized by alpha-lower motor neuron loss and muscle atrophy, however, there is a growing list of tiss

179 son of gene expression in hibernation versus muscle atrophy identified several genes differentially r

180 mon, unidentified receptor to block skeletal muscle atrophy in a GH-independent manner.

181 r UnAG and AG could protect against skeletal muscle atrophy in a GHSR-1a-independent manner.

182 reduction in PGE(2) signaling contributed to muscle atrophy in aged mice and results from 15-PGDH-exp

183 ssion, downregulated Akt phosphorylation and muscle atrophy in ALS and clearly demonstrates a direct

184 Decreased Akt activity is linked to muscle atrophy in ALS and is associated with increased a

185 p53 family target genes and the severity of muscle atrophy in ALS patients and mice.

186 lucocorticoid-induced insulin resistance and muscle atrophy in C2C12 myotubes.

187 PDK4 drives metabolic alterations and muscle atrophy in cancer cachexia.

188 However, the molecular mechanisms of muscle atrophy in CHF and their interaction with aging a

189 ng role in increased protein degradation and muscle atrophy in insulin-deficient diabetes.

190 Elevated miR-542-3p/5p may cause muscle atrophy in intensive care unit patients through t

191 been associated with chronic weight loss and muscle atrophy in mice.

192 ripe tomatoes, inhibits age-related skeletal muscle atrophy in mice.

193 Physical inactivity generates muscle atrophy in most mammalian species.

194 Angiotensin (Ang) II induces skeletal muscle atrophy in part by increased muscle-enriched E3 u

195 Here we show that miR-29b promotes skeletal muscle atrophy in response to different atrophic stimuli

196 the first study to demonstrate that skeletal muscle atrophy in response to disuse is accompanied by d

197 88-knockout (wbMyD88KO) mice resist skeletal muscle atrophy in response to LPS, muscle-specific delet

198 ronal nitric oxide synthase (nNOS) regulates muscle atrophy in skeletal muscle.

199 k of cast immobilization induced significant muscle atrophy in Sol but not in EDL.

200 ar injection of AAV1-follistatin ameliorates muscle atrophy in suboptimally dosed Delta7 mice.

201 a is a wasting condition defined by skeletal muscle atrophy in the setting of systemic inflammation.

202 1 increases during inflammation and mediates muscle atrophy in vivo.

203 result, Gadd45a reduces multiple barriers to muscle atrophy (including PGC-1alpha, Akt activity, and

204 We instead see hallmarks of muscle atrophy, including an ordered disassembly of the

205 were associated with significantly decreased muscle atrophy, increased myofiber diameter, and improve

206 new therapeutic agents to prevent or reduce muscle atrophy induced by denervation of diverse etiolog

207 29b may represent a therapeutic approach for muscle atrophy induced by different stimuli.

208 f circulating UnAG in mice impaired skeletal muscle atrophy induced by either fasting or denervation

209 In mice, during the rapid muscle atrophy induced by fasting, the desmin cytoskelet

210 ction of MAFbx/Atrogin-1 mRNA expression and muscle atrophy induced by glucocorticoid.

211 e show that Gadd45a is required for skeletal muscle atrophy induced by three distinct skeletal muscle

212 Muscle atrophy, insulin resistance and reduced muscle ph

213 Muscle atrophy involves a common pattern of transcriptio

214 Previous work found that skeletal muscle atrophy involves an increase in skeletal muscle G

215 neuron dysfunction leads to target skeletal muscle atrophy involving dysregulation of downstream cel

216 Skeletal muscle atrophy is a common and debilitating condition th

217 neurodegenerative disorder of which skeletal muscle atrophy is a common feature, and multiple lines o

218 Skeletal muscle atrophy is a highly-prevalent and debilitating co

219 X-linked myopathy with postural muscle atrophy is a novel X-linked myopathy caused by mu

220 Muscle atrophy is a physiological response to disuse and

221 Skeletal muscle atrophy is a serious and highly prevalent conditi

222 Skeletal muscle atrophy is a severe condition of muscle mass loss

223 Skeletal muscle atrophy is also considerable in type 1 diabetes,

224 Sustained muscle atrophy is associated with decreased satellite ce

225 Muscle atrophy is caused by a down-regulation of protein

226 Muscle atrophy is regulated by the balance between prote

227 A hallmark of muscle atrophy is the excessive degradation of myofibril

228 riction injury to a nerve and the associated muscle atrophy is unclear.

229 biochemical mechanism by which ATF4 promotes muscle atrophy is unknown.

230 Sarcopenia, or skeletal muscle atrophy, is a debilitating comorbidity of many ph

231 ypomyelination in the Lkb1-mutant nerves and muscle atrophy lead to hindlimb dysfunction and peripher

232 Despite insulin resistance and muscle atrophy, M-p110alphaKO mice show decreased serum

233 In addition, a muscle atrophy marker, myostatin, is increased in UUO mu

234 pecific RING finger protein-1 and atrogin-1, muscle atrophy markers, was decreased by 79 and 88%, res

235 e have recently shown that T. gondii-induced muscle atrophy meets the clinical definition of cachexia

236 we show that loss of innervation in several muscle atrophy models including aging induces generation

237 of age prevented body weight loss, skeletal muscle atrophy, muscle weakness, contractile abnormaliti

238 During muscle atrophy, myofibrillar proteins are degraded in an

239 Robust skeletal muscle atrophy occurs after burn injury, even in muscles

240 ovide new insight into the way that skeletal muscle atrophy occurs at the molecular level.

241 Following this surgery, considerable muscle atrophy occurs, resulting in decreased strength a

242 d if secondary radiological findings such as muscle atrophy, oedema in peripheric soft tissue and bon

243 nown to induce severe systemic bone loss and muscle atrophy of astronauts due to the circumstances of

244 CMT is usually characterized by distal muscle atrophy, often with foot deformity, weakness and

245 xpression of Fn14 is a rate-limiting step in muscle atrophy on denervation, mechanisms regulating gen

246 Fasciculation without weakness, muscle atrophy or increased tendon reflexes suggests a b

247 to modulate gene expression during skeletal muscle atrophy or recovery have yet to be investigated.

248 and other disorders with focal or asymmetric muscle atrophy or weakness.

249 neuron 1 gene leading to motor neuron loss, muscle atrophy, paralysis, and death.

250 which motor neurons degenerate, resulting in muscle atrophy, paralysis, and fatality.

251 ube formation through activation of skeletal muscle atrophy pathways.

252 X-linked myopathy with postural muscle atrophy patients consistently showed electrical,

253 CT: Severe burns result in profound skeletal muscle atrophy; persistent muscle atrophy and weakness a

254 Severe burns result in profound skeletal muscle atrophy; persistent muscle loss and weakness are

255 mizygous male Mtm1 p.R69C mice develop early muscle atrophy prior to the onset of weakness at 2 month

256 nveil that BET proteins directly promote the muscle atrophy program during cachexia.

257 ecapitulates HDAC4 deficiency and blunts the muscle atrophy program.

258 cal mechanism by which ATF4 induces skeletal muscle atrophy, providing molecular-level insights into

259 rgery was inversely related to the degree of muscle atrophy (r = 0.65, P < 0.01).

260 rised E3 ubiquitin ligase (UBR5) in skeletal muscle atrophy, recovery from atrophy and injury, anabol

261 haracterized E3 ubiquitin ligase in skeletal muscle atrophy, recovery from atrophy/injury, anabolism

262 ed diaphragmatic dysfunction, which includes muscle atrophy, reduced force development, and impaired

263 Susceptibility to age-related muscle atrophy relates to the degree of muscle denervati

264 Mapping the transcriptional regulation of muscle atrophy requires an unbiased analysis of the whol

265 MN1) gene, which leads to motor neuron loss, muscle atrophy, respiratory distress, and death.

266 eletion of both transporters caused skeletal muscle atrophy, resulting in death by postnatal day P13.

267 dy myopathy, X-linked myopathy with postural muscle atrophy, rigid spine syndrome (RSS) and Emery-Dre

268 tion of the OOM and histological evidence of muscle atrophy similar to groups 1 and 2.

269 oped motor and gait deficits with underlying muscle atrophy, similar to that observed in the constitu

270 cle atrophy, enhanced recovery from skeletal muscle atrophy, stimulated skeletal muscle hypertrophy,

271 upregulation of other factors implicated in muscle atrophy, such as angiotensin-II, activin and Acvr

272 ermore, mGRKO mice exhibit 77% less skeletal muscle atrophy than control animals in response to tumor

273 been shown to play a more important role in muscle atrophy than previously recognized.

274 Severe burns result in profound skeletal muscle atrophy that hampers recovery.

275 show that MuRF1 is responsible for mediating muscle atrophy that occurs during the period of active l

276 During muscle atrophy, the E3 ligase atrogenes, atrogin-1 and m

277 kely contribute to the attenuation of disuse muscle atrophy through prolonged periods of immobility o

278 y, our study demonstrates that TWEAK induces muscle atrophy through repressing the levels of PGC-1alp

279 use of exercise-generated metabolite AKG in muscle atrophy treatment, but also identify PHD3 as a po

280 e expression of Fn14 and attenuates skeletal muscle atrophy upon denervation.

281 de evidence that high CO2 activates skeletal muscle atrophy via AMPKalpha2-FoxO3a-MuRF1, which is of

282 n of Smad1/5 exacerbated denervation-induced muscle atrophy via an HDAC4-myogenin-dependent process,

283 fasting, and immobilization promote skeletal muscle atrophy via expression of activating transcriptio

284 hat miR-29b contributes to multiple types of muscle atrophy via targeting of IGF-1 and PI3K(p85alpha)

285 Fasting-induced muscle atrophy was also compromised in female MBKO mice,

286 X-linked myopathy with postural muscle atrophy was associated with reduced exercise capa

287 Muscle atrophy was not ameliorated by intensive insulin

288 hese results, relatively less DNA damage and muscle atrophy was observed in Myostatin(-/-) muscle in

289 Change in quadriceps muscle atrophy was significantly associated with change

290 mechanism by which Gadd45a promotes skeletal muscle atrophy was unknown.

291 To identify potential mechanisms underlying muscle atrophy, we studied the impact of VDR knockdown (

292 gmented mitochondria, glial cell activation, muscle atrophy, weight loss, and reduced survival.

293 Axonal degeneration in the spinal cord and muscle atrophy were also observed, along with accumulati

294 t against the inflammation-mediated skeletal muscle atrophy which occurs in sarcopenia and cachexia.

295 in the development and pathology of skeletal muscle atrophy, which is common in patients with endothe

296 nervation of skeletal muscles induces severe muscle atrophy, which is preceded by cellular alteration

297 is a potential novel factor associated with muscle atrophy, which may become a therapeutic target in

298 -29b overexpression is sufficient to promote muscle atrophy while inhibition of miR-29b attenuates at

299 Skeletal muscle atrophy with reduced strength, severe sarcomere d

300 ceiving placebo exhibited greater quadriceps muscle atrophy, with a -14.3 +/- 3.6% change from baseli