ライフサイエンスコーパス: muscle atrophy

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

2 tic to ameliorate the deleterious effects of muscle atrophy.

3 tosis, microgliosis and ameliorates skeletal muscle atrophy.

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

5 mRNA expression signatures of human skeletal muscle atrophy.

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

7 be elevated in several settings of skeletal muscle atrophy.

8 urons, resulting in progressive weakness and muscle atrophy.

9 rapeutic agent or lead compound for skeletal muscle atrophy.

10 al regulator of denervation-induced skeletal muscle atrophy.

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

12 patients and mice with inflammation-induced muscle atrophy.

13 1 and Atrogin-1, and progression of skeletal muscle atrophy.

14 echanism through which Dex promotes skeletal muscle atrophy.

15 ation resulting in vacuolation, weakness and muscle atrophy.

16 ific CuZnSOD deletion is sufficient to cause muscle atrophy.

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

18 tion factors whose activation is critical in muscle atrophy.

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

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

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

22 r remodeling and a comprehensive program for muscle atrophy.

23 degradation of myofibrillar proteins during muscle atrophy.

24 egeneration of spinal cord motor neurons and muscle atrophy.

25 starvation and muscle disuse cause skeletal muscle atrophy.

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

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

28 of muscle growth in diseases associated with muscle atrophy.

29 haracterized by motor neuron loss and severe muscle atrophy.

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

31 l muscle protein metabolism, and progressive muscle atrophy.

32 ough cytokine-activated pathways, leading to muscle atrophy.

33 tments successfully block the development of muscle atrophy.

34 Weakness is not simply a matter of muscle atrophy.

35 otor nerve conduction velocities (MNCVs) and muscle atrophy.

36 in models of acute and chronic inflammatory muscle atrophy.

37 motor neurons, such that denervation causes muscle atrophy.

38 cally evaluated for generalized weakness and muscle atrophy.

39 progressive genes were also associated with muscle atrophy.

40 increases mitochondrial content and inhibits muscle atrophy.

41 dinates AT-1 and ubiquitin expression during muscle atrophy.

42 in skeletal muscle protects from CKD-induced muscle atrophy.

43 ant deregulation of pathways associated with muscle atrophy.

44 ttenuation of inflammation-mediated skeletal muscle atrophy.

45 caspase-mediated proteolysis contributes to muscle atrophy.

46 teolysis helps explain how exercise prevents muscle atrophy.

47 ompensatory mitochondrial proliferation, and muscle atrophy.

48 ed PI3K activity in muscle and did not cause muscle atrophy.

49 ss, whereas nitric oxide may protect against muscle atrophy.

50 of neurons, decreased myelination, and mild muscle atrophy.

51 ated PI3K activity in muscle and progressive muscle atrophy.

52 in NF-kappaB activity is required for disuse muscle atrophy.

53 D2 leads to accelerated aging, blindness and muscle atrophy.

54 thyl N-nitrosourea-induced mouse mutant with muscle atrophy.

55 ochondria may be an important determinant of muscle atrophy.

56 e necessary and sufficient for physiological muscle atrophy.

57 d to cause human cardiomyopathy and skeletal muscle atrophy.

58 kinases of the IKK complex are required for muscle atrophy.

59 ophy signaling pathways and prevent skeletal muscle atrophy.

60 ysregulated metabolic functions and signs of muscle atrophy.

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

62 aracterized by motor neuron degeneration and muscle atrophy.

63 the treatment of conditions which result in muscle atrophy.

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

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

66 uced insulin resistance, taking into account muscle atrophy.

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

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

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

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

71 igated whether hypercapnia leads to skeletal muscle atrophy.

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

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

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

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

76 Synapses eventually denervate and the muscles atrophy.

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

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

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

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

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

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

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

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

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

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

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

88 nase values (average 4500 IU/l) and frequent muscle atrophy and asymmetry of muscle involvement.

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

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

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

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

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

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

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

96 6'-sialyllactose ameliorated muscle atrophy and degeneration in symptomatic GNE myopa

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

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

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

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

101 nding the physiological processes underlying muscle atrophy and hypertrophy.

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

103 /FOXO1 signalling, and therefore prevent the muscle atrophy and impairment of carbohydrate oxidation.

104 x O 1 (FOXO1) signalling in the induction of muscle atrophy and impairment of muscle carbohydrate oxi

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

106 s, MuRF1 and MAFbx, are excellent markers of muscle atrophy and increase under divergent atrophy-indu

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

108 s study reveals a novel mediator of skeletal muscle atrophy and indicates that the TWEAK-Fn14 system

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

110 nges in FOXO-dependent processes influencing muscle atrophy and insulin resistance during sepsis.

111 Sepsis causes muscle atrophy and insulin resistance, but the underlyin

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

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

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

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

116 a complex adaptive response that results in muscle atrophy and loss of specific force.

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

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

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

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

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

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

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

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

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

126 14 axis in IBM muscle may induce progressive muscle atrophy and reduce activation and differentiation

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

128 study unveils a novel mechanism of skeletal muscle atrophy and suggests that TRAF6 is an important t

129 In support of this, muscle atrophy and the Amplex Red signal are inhibited i

130 e Dex infusion during endotoxaemia prevented muscle atrophy and the impairment of carbohydrate oxidat

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

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

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

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

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

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

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

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

139 eneration of lower motor neurons, leading to muscle atrophy and, in the most severe cases, paralysis

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

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

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

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

144 f cancer cachexia, they significantly reduce muscle atrophy, and inhibit muscle protein loss and DNA

145 bnormalities of the neuromuscular junctions, muscle atrophy, and motor neuron degeneration.

146 otor neurons, denervation of target muscles, muscle atrophy, and paralysis.

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

148 aciopharyngeal weakness, usually with marked muscle atrophy, and relatively isolated neck extensor an

149 nerative disorder characterized by weakness, muscle atrophy, and spasticity, is the most common adult

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

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

152 Mechanisms of muscle atrophy are complex and their understanding might

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

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

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

156 Reversing muscle atrophy associated with SMA may represent an unex

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

158 4 (CXCR4) pathway were downregulated only in muscles atrophying because of cancer: stromal cell-deriv

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

160 s characterized by loss of motor neurons and muscle atrophy, but the initial cellular events that pre

161 ally ill patients experience marked skeletal muscle atrophy, but the molecular mechanisms responsible

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

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

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

165 Protection from wasting and muscle atrophy by CD4(+)CD44(v.low) cells is associated

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

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

168 Muscle atrophy (cachexia) in cancer patients is a life-t

169 These included shortening of the limbs, muscle atrophy, cartilage dysplasia, and immature bone.

170 itical factor underlying the severe skeletal muscle atrophy characteristic of muscle fibers in patien

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

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

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

174 Skeletal muscle atrophy due to excessive protein degradation is t

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

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

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

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

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

180 the pharmacokinetics of the statin response, muscle atrophy, exercise intolerance, pain perception, a

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

182 did not prevent the LPS-mediated increase in muscle atrophy F-box (MAFbx) and muscle RING finger 1 (M

183 were accompanied by significant increases in muscle atrophy F-box mRNA (5.5-fold, P < 0.001) and prot

184 muscle-specific ring finger 1, and atrogin-1/muscle atrophy F-box were lower in mXIAP-CKD mice, sugge

185 Atrogin-1, also known as muscle atrophy F-box, is an F-box protein that inhibits

186 skeletal muscle of HDAC mutant mice restores muscle atrophy following denervation.

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

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

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

190 order characterized by motor neuron loss and muscle atrophy, has been linked to mutations in the Surv

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

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

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

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

195 apacity may contribute to the progression of muscle atrophy in ALS.

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

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

198 hat myocardial myostatin expression controls muscle atrophy in heart failure.

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

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

201 rly understood event leading to weakness and muscle atrophy in motor neuron diseases.

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

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

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

205 88-knockout (wbMyD88KO) mice resist skeletal muscle atrophy in response to LPS, muscle-specific delet

206 In the present study, we demonstrate that muscle atrophy in Sod1(-/-) mice is accompanied by a pro

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

208 myopathic changes and, indeed, caused severe muscle atrophy in Tg(Pkd1l2)/Tg(Pkd1l2) mice.

209 Moreover, muscle atrophy in the A17.1 mice was restricted to fast

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

211 ults demonstrate a fibre-type specificity of muscle atrophy in this OPMD model.

212 1 increases during inflammation and mediates muscle atrophy in vivo.

213 in-1, a gene required for the development of muscle atrophy, in statin-induced muscle damage.

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

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

216 29b may represent a therapeutic approach for muscle atrophy induced by different stimuli.

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

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

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

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

221 Muscle atrophy involves a common pattern of transcriptio

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

223 Skeletal muscle atrophy is a common and debilitating condition th

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

225 Muscle atrophy is a consequence of chronic diseases (e.g

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

227 Skeletal muscle atrophy is a serious and highly prevalent conditi

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

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

230 Sustained muscle atrophy is associated with decreased satellite ce

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

232 etween the biology of muscular dystrophy and muscle atrophy is elucidated (see the related study begi

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

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

235 ery from critical illnesses including disuse muscle atrophy, joint contractures, thromboembolic disea

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

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

238 enotype by slowing or reversing the skeletal muscle atrophy may also be beneficial.

239 to cause "JMP" syndrome (joint contractures, muscle atrophy, microcytic anemia, and panniculitis-indu

240 yndrome characterized by joint contractures, muscle atrophy, microcytic anemia, and panniculitis-indu

241 In adults, muscle atrophy, muscle dysfunction, and muscle weakness

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

243 During muscle atrophy, myofibrillar proteins are degraded in an

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

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

246 Skeletal muscle atrophy occurs in a variety of clinical settings,

247 Skeletal muscle atrophy occurs under a variety of conditions and

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

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

250 ssessed global damage, serum creatinine, and muscle atrophy on magnetic resonance imaging, and in juv

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

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

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

254 ube formation through activation of skeletal muscle atrophy pathways.

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

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

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

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

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

260 ecapitulates HDAC4 deficiency and blunts the muscle atrophy program.

261 Furthermore, GW610742 initiated a muscle atrophy programme, possibly via changes in the Ak

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

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

264 In certain models of muscle atrophy, reduced satellite cell function contribu

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

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

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

268 Cachexia is the dramatic weight loss and muscle atrophy seen in chronic disease states, including

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

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 ucer of apoptosis (TWEAK), mediates skeletal muscle atrophy that occurs under denervation conditions.

277 sive neurological deterioration and skeletal muscle atrophy that resemble those seen in HD patients.

278 Despite their well-characterised roles in muscle atrophy, the dynamics of MURF expression in the d

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

280 chectic cancer patients, which would lead to muscle atrophy through a depression in protein synthesis

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

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

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

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

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

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

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

288 Muscle atrophy was not ameliorated by intensive insulin

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

290 Change in quadriceps muscle atrophy was significantly associated with change

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

292 ignaling has been tightly linked to skeletal muscle atrophy, we hypothesize that loss of Akt-dependen

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

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

295 portance of Hsp70 expression during skeletal muscle atrophy, when Hsp70 levels are significantly decr

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

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

300 aB) signaling is necessary for many types of muscle atrophy, yet only some of the required components