ライフサイエンスコーパス: muscle wasting

1 ed by increased glucagon, without preventing muscle wasting.

2 ions that disrupt this activity cause severe muscle wasting.

3 hes in cell-based therapy to combat skeletal muscle wasting.

4 CU acquired paresis and other forms of acute muscle wasting.

5 a class of disorders that cause progressive muscle wasting.

6 e necessary and sufficient for tumor-induced muscle wasting.

7 tive function describes two major aspects of muscle wasting.

8 acterized by chronic inflammation and severe muscle wasting.

9 entify their role in ALI-associated skeletal muscle wasting.

10 activation of the Akt pathway to counteract muscle wasting.

11 cohol-induced accentuation of SIV-associated muscle wasting.

12 mour-induced atrogin1/MAFbx upregulation and muscle wasting.

13 LLC) induces atrogin1/MAFbx upregulation and muscle wasting.

14 conditions are sufficient to cause profound muscle wasting.

15 an important target for preventing skeletal muscle wasting.

16 ulation is temporally correlated with severe muscle wasting.

17 rtant therapeutic target to prevent skeletal muscle wasting.

18 al therapeutic targets to reduce CKD-related muscle wasting.

19 or-beta superfamily that is known to control muscle wasting.

20 g an improved side effect profile in IOP and muscle wasting.

21 g, providing a method for early detection of muscle wasting.

22 nce on glucocorticoid treatment but not from muscle wasting.

23 s might be a therapeutic approach to prevent muscle wasting.

24 uring atrophy, and MuRF1 deletion attenuates muscle wasting.

25 netic disorders characterized by progressive muscle wasting.

26 nd targeting TLR4 alone effectively abrogate muscle wasting.

27 hin thereby preventing sarcolemma damage and muscle wasting.

28 generation of lower motor neurons leading to muscle wasting.

29 target for the development of therapies for muscle wasting.

30 ed progressive spastic paraplegia and distal muscle wasting.

31 pecific splicing or cytoplasmic functions in muscle wasting.

32 er degeneration/regeneration and progressive muscle wasting.

33 gical consequence of many diseases involving muscle wasting.

34 osin in conditions such as heart failure and muscle wasting.

35 , which is associated with hyperglycemia and muscle wasting.

36 functional, and structural events, including muscle wasting.

37 ocorticoid-regulated molecular mechanisms of muscle wasting.

38 including marked facial weakness and tongue muscle wasting.

39 t in the progression of a catabolic state in muscle wasting.

40 new targets for the therapeutic treatment of muscle wasting.

41 that their misregulation causes the dramatic muscle wasting.

42 of the renin-angiotensin system and skeletal muscle wasting.

43 d at the onset and during the progression of muscle wasting.

44 pha-II is a potential therapeutic target for muscle wasting.

45 factors is an attractive approach to combat muscle wasting.

46 e responsible for tumor's capacity to induce muscle wasting.

47 tor and therapeutic target of cancer-induced muscle wasting.

48 hic mice, likely as a consequence of chronic muscle wasting.

49 the effect of selected miRNAs on age-related muscle wasting.

50 signaling suggest novel approaches to combat muscle wasting.

51 /HDAC5/TFEB/MuRF1 pathway to induce skeletal muscle wasting.

52 atic amino acid catabolism without affecting muscle wasting.

53 t repress skeletal muscle growth and promote muscle wasting.

54 al myocytes were resistant to Ang II-induced muscle wasting.

55 ation or tenotomy did not prevent subsequent muscle wasting.

56 activation of HDAC6 in mice protects against muscle wasting.

57 d across different modes of non-degenerative muscle wasting.

58 istatin-based therapies for non-degenerative muscle wasting.

59 muscle, which is required for prevention of muscle wasting.

60 and the basal lamina, leading to progressive muscle wasting.

61 portunities for the treatment of progressive muscle wasting.

62 tress might reduce the rate of bone loss and muscle wasting.

63 ar dystrophy with early-onset of progressive muscle-wasting.

64 bjective Global Assessment, experienced less muscle wasting (0.43 vs 0.27 score increase per week; me

65 epresses skeletal muscle growth and promotes muscle wasting, a role in muscle for the parallel bone m

66 Muscle wasting, also known as cachexia, is associated wi

67 in the onset and progression of age-related muscle wasting, also known as sarcopenia, and discusses

68 Muscle wasting and cachexia have long been postulated to

69 possible pharmacological approach to prevent muscle wasting and cachexia.

70 function leads to myopathy, characterized by muscle wasting and cardiac hypertrophy.

71 ack of nourishment inevitably led to massive muscle wasting and death in double-knockout animals.

72 nfusion in rodents causes sustained skeletal muscle wasting and decreases muscle regenerative potenti

73 in nuclear foci and its expression leads to muscle wasting and degeneration in Drosophila.

74 Muscle wasting and diminished physical performance often

75 RATIONALE: Critical illness is hallmarked by muscle wasting and disturbances in glucose, lipid, and a

76 atures, with diabetes, deafness, progressive muscle wasting and ectopic calcifications specifically o

77 tical role for NF-kappaB in the pathology of muscle wasting and establishing it as an important clini

78 it disease phenotypes such as cancer-related muscle wasting and fibrosis.

79 osis (TWEAK) is a potent inducer of skeletal muscle wasting and fibrosis.

80 ection had significantly less spasticity and muscle wasting and greater mobility at the hip, knee, an

81 eneous late-onset disease involving skeletal muscle wasting and heart defects caused, in a minority o

82 nstrate the implication of HDAC6 in skeletal muscle wasting and identify HDAC6 as a new downstream ta

83 re fully fed contribute to bone and skeletal muscle wasting and impose risk of adrenocortical atrophy

84 this potent cytokine could contribute to the muscle wasting and insulin resistance that are character

85 harboring Mtm1 mutations remarkably rescued muscle wasting and lethality, and this effect was muscle

86 y in adults, is characterized by progressive muscle wasting and multi-systemic complications.

87 MBNL1, leading to clinical symptoms such as muscle wasting and myotonia.

88 ms being severe muscle weakness, progressive muscle wasting and myotonia.

89 id the development of therapeutics to combat muscle wasting and neuromuscular disorders.

90 uscle disorders characterized by progressive muscle wasting and often premature death.

91 eath of motor neurons leading to spasticity, muscle wasting and paralysis.

92 y upper and lower motor neuron degeneration, muscle wasting and paralysis.

93 These findings reveal a specific pathway for muscle wasting and potential therapeutic targets for thi

94 the absence of dystrophin causes progressive muscle wasting and premature death.

95 ons for understanding mechanisms of skeletal muscle wasting and provide a rationale for new therapeut

96 ostmyocardial infarction, there was skeletal muscle wasting and reduced SC numbers that were inhibite

97 ferent mechanisms are involved in pathologic muscle wasting and that autophagy, either excessive or d

98 rophy, which is characterised by progressive muscle wasting and the discovery of reliable blood-based

99 increased in the quadriceps of patients with muscle wasting and to determine the molecular pathways b

100 llowed by a catabolic response that leads to muscle wasting and weakness affecting skeletal musculatu

101 euron (LMN) syndromes typically present with muscle wasting and weakness and may arise from pathology

102 s are elevated in disorders characterized by muscle wasting and weakness, such as inflammatory myopat

103 who are on hemodialysis commonly experience muscle wasting and weakness, which have a negative effec

104 tegies to treat, or even prevent, peripheral muscle wasting and weakness.

105 e group of diseases characterized by chronic muscle wasting and weakness.

106 of muscle diseases characterized by skeletal muscle wasting and weakness.

107 induced hypoaminoacidemia, without affecting muscle wasting and without a sustained impact on blood g

108 erse group of genetic disorders that lead to muscle wasting and, in many instances, premature death.

109 are a group of genetic diseases that lead to muscle wasting and, in most cases, premature death.

110 been identified that are involved in various muscle-wasting and neuromuscular disorders.

111 implicated in the pathogenesis of cachexia (muscle wasting) and the hallmark symptom, exercise intol

112 with features of ataxia, paralysis, skeletal muscle wasting, and degeneration.

113 d role for electrical activity in regulating muscle wasting, and indicate that muscle disuse induces

114 ng heart failure, cardiac pacemaker defects, muscle wasting, and osteoporosis, in heart, skeletal mus

115 iated with motor neuron degeneration, severe muscle wasting, and premature death by 6 mo of age.

116 In mice, miR-542 overexpression caused muscle wasting, and reduced mitochondrial function, 12S

117 eam effector of IL-6, are also elevated with muscle wasting, and STAT3 has been implicated in the reg

118 urn trauma, with a focus on hypermetabolism, muscle wasting, and stress-induced diabetes.

119 Metabolic acidosis promotes muscle wasting, and the net acid load from diets that ar

120 ultiple factors contribute to cancer-induced muscle wasting, and therefore therapy requires combinati

121 Common clinical manifestations include muscle wasting, anemia, reduced caloric intake, and alte

122 Several mouse models of skeletal muscle wasting are associated with lipin1 mutation or al

123 ation of ubiquitin ligase atrogin1/MAFbx and muscle wasting are hallmarks of cancer cachexia; however

124 ntly, new therapies that can safely suppress muscle wasting are needed.

125 Skeletal muscle wasting as a direct consequence of critical illne

126 mplications as encephalopathy, malnutrition, muscle wasting, ascites, esophagogastric variceal hemorr

127 has been shown in developing a treatment of muscle wasting associated with a range of diseases as we

128 Caspase-3 contributes to the muscle wasting associated with chronic kidney disease (C

129 e pathway is the principal cause of skeletal muscle wasting associated with common human disease stat

130 muscle phenotype, which could contribute to muscle wasting associated with metabolic disorders.

131 yofiber immunoglobulin G uptake, and reduced muscle wasting at 3 and 6 months after treatment.

132 ith that of two ubiquitin ligases induced in muscle wasting, atrogin-1 and MuRF1, suggesting a possib

133 Skeletal muscle wasting attributed to inactivity has significant

134 Cancer-induced muscle wasting begins early in the course of a patient's

135 of ActRIIB pathway not only prevents further muscle wasting but also completely reverses prior loss o

136 e been proposed as therapeutics for treating muscle wasting but concerns regarding possible off-targe

137 d simply to the degree of lower motor neuron muscle wasting but, rather, depend on the pathophysiolog

138 glucose and lipid metabolism, did not affect muscle wasting, but drastically suppressed markers of he

139 SIRT1 overexpression reduces muscle wasting by blocking the activation of FoxO1 and 3

140 ke receptor 4 (TLR4) mediates cancer-induced muscle wasting by directly activating muscle catabolism

141 C-1alpha levels in skeletal muscle prevented muscle wasting by reducing apoptosis, autophagy, and pro

142 Inactivity causes muscle wasting by triggering protein degradation and may

143 Muscle wasting (cachexia) is an incurable complication a

144 causes muscle membrane instability, skeletal muscle wasting, cardiomyopathy, and heart failure.

145 With muscle wasting, caspase-3 activation and the ubiquitin-p

146 odulated to prevent neuronal dysfunction and muscle wasting caused by protein misfolding in HD.

147 s) are promising biomarkers of the inherited muscle wasting condition Duchenne muscular dystrophy, as

148 Indeed, we found that in mice with a muscle wasting condition, chronic kidney disease, there

149 rapeutic approach to improve regeneration in muscle wasting conditions.

150 d provide a clinically useful way to monitor muscle-wasting conditions.

151 odels in which to study extremely aggressive muscle-wasting conditions.

152 6), are associated with both age-related and muscle-wasting conditions.

153 of apoptosis (TWEAK), a recently identified muscle-wasting cytokine, on the expression of extracellu

154 tor-1 did not recover in those who developed muscle wasting (day 7 compared with baseline, p<0.01) bu

155 as sustained at day 7 in those who developed muscle wasting (day 7 compared with baseline, p<0.01), b

156 ceptor on skeletal muscle and thereby induce muscle wasting described as cachexia.

157 infection and neurodegenerative disorders to muscle wasting, diabetes and inflammation.

158 ne muscular dystrophy (DMD) is a devastating muscle wasting disease caused by mutations in dystrophin

159 ar dystrophy (BMD) is a progressive X-linked muscle wasting disease for which there is no treatment.

160 Muscular dystrophy is a progressive muscle wasting disease that is thought to be initiated b

161 causes Duchenne muscular dystrophy, a lethal muscle wasting disease.

162 scular dystrophy (DMD) is a lethal, X-linked muscle-wasting disease caused by lack of the cytoskeleta

163 lar dystrophy (DMD) is an incurable X-linked muscle-wasting disease caused by mutations in the dystro

164 dystrophy (DMD) is a severe and progressive muscle-wasting disease caused by mutations in the dystro

165 y no effective treatment for the devastating muscle-wasting disease Duchenne muscular dystrophy (DMD)

166 e muscular dystrophy is a rare, progressive, muscle-wasting disease leading to severe disability and

167 dystrophy (DMD) is the most common, lethal, muscle-wasting disease of childhood.

168 scular dystrophy type 1A (MDC1A) is a lethal muscle-wasting disease that is caused by mutations in th

169 trophy type 1A (MDC1A) is a severe and fatal muscle-wasting disease with no cure.

170 Duchenne muscular dystrophy (DMD), a genetic muscle-wasting disease.

171 scular dystrophies are broadly classified as muscle wasting diseases with myofiber dropout due to cel

172 ibition is therefore a potential therapy for muscle wasting diseases, some of which are associated wi

173 armacological properties for use in treating muscle wasting diseases.

174 le, enabling future cell-based therapies for muscle-wasting diseases.

175 enous regenerative response and ameliorating muscle-wasting diseases.

176 Duchenne muscular dystrophy (DMD) is a fatal muscle wasting disorder caused by mutations in the dystr

177 strophy is a severe and progressive striated muscle wasting disorder that leads to premature death fr

178 s such, it is a prime therapeutic target for muscle wasting disorders.

179 gene underlie a group of autosomal recessive muscle-wasting disorders denoted as dysferlinopathies.

180 ults in further cohorts with these and other muscle-wasting disorders would suggest that MRI biomarke

181 exarotene in the prevention and treatment of muscle-wasting disorders, particularly given the lack of

182 f muscle growth and a therapeutic target for muscle-wasting disorders.

183 itors that could be used in the treatment of muscle-wasting disorders.

184 re also elevated in the serum of progressive muscle wasting DM1 patients compared to disease-stable D

185 In addition to skeletal muscle wasting, DMD patients develop cardiomyopathy, whi

186 umor-bearing TLR4(-/-) mice were spared from muscle wasting due to a blockade in muscle catabolic pat

187 tophagic-lysosomal, calpain, and caspase) in muscle wasting during cancer cachexia.

188 ng protein response pathways causes skeletal muscle wasting during cancer cachexia.

189 se, lipid, and amino acid homeostasis and in muscle wasting during critical illness.

190 , hypogonadism, infertility, severe skeletal muscle wasting, emphysema, and osteopenia, as well as ge

191 nic heart failure often results in catabolic muscle wasting, exercise intolerance, and death.

192 In a novel human model of acute muscle wasting following cardiac surgery, known or poten

193 es a specific method to identify obesity and muscle wasting for end-stage liver disease patients.

194 ory cytokines are known to cause significant muscle wasting, however, their role in myofiber regenera

195 -like phenotypes, including kyphosis, severe muscle wasting, hypogonadism, osteopenia, emphysema, unc

196 ft tissue and vascular calcification, severe muscle wasting, hypogonadism, pulmonary emphysema, diste

197 n mdx mice restored their longevity, reduced muscle wasting, improved function and greatly increased

198 e analyzed the effects of glucocorticoids on muscle wasting in a mouse model of acute diabetes.

199 investigated the clinical course of skeletal muscle wasting in advanced cancer and the window of poss

200 llmark associated with neurodegeneration and muscle wasting in Alzheimer's disease (AD) and inclusion

201 ells in the muscle microenvironment to drive muscle wasting in cancer.

202 There are no approved therapies for muscle wasting in children infected with human immunodef

203 e changes in pathways that may contribute to muscle wasting in chronic binge alcohol-fed SIV-infected

204 ocess is a critical determinant for skeletal muscle wasting in chronic diseases and degenerative musc

205 peutic avenue for the prevention of skeletal muscle wasting in chronic heart failure and potentially

206 Muscle wasting in chronic kidney disease (CKD) begins wi

207 The etiology of muscle wasting in chronic obstructive pulmonary disease

208 stemic illnesses, but whether XIAP modulates muscle wasting in CKD is unknown.

209 ular signatures of processes associated with muscle wasting in CKD, including proteolysis, myogenesis

210 findings may provide insights into skeletal muscle wasting in critical illness.

211 ar biomarkers for monitoring the progress of muscle wasting in DM1 patients.

212 iRNAs are associated with the progression of muscle wasting in DM1 patients.

213 uscle regeneration are major contributors to muscle wasting in Duchenne muscular dystrophy (DMD).

214 de therefore offers a strategy for reversing muscle wasting in Duchenne's muscular dystrophy (DMD) wi

215 ) magnetic resonance imaging (MRI) to assess muscle wasting in facial and tongue muscles.

216 ar S1P elevation promotes the suppression of muscle wasting in flies.

217 tial therapeutic target for the treatment of muscle wasting in heart failure, we infused a myostatin

218 eleased from cardiomyocytes induces skeletal muscle wasting in heart failure.

219 ults in reduced growth, ataxia, and hindlimb muscle wasting in mice.

220 ing Hsp70 and Hsp90 as key cachexins causing muscle wasting in mice.Cachexia affects many cancer pati

221 instability, a common mechanism of skeletal muscle wasting in muscular dystrophies.

222 The extent of muscle wasting in MuSK-MG, and whether it is also found

223 Insulin resistance is a major cause of muscle wasting in patients with ESRD.

224 ession or absence of TP53INP2 did not affect muscle wasting in response to denervation, a condition i

225 on of myogenesis in vitro and contributes to muscle wasting in response to tumor load in vivo.

226 vels and cachexia and Ang II causes skeletal muscle wasting in rodents, the potential effects of Ang

227 verexpression of Tp53inp2 exhibited enhanced muscle wasting in streptozotocin-induced diabetes that w

228 Acute muscle wasting in the critically ill is common and cause

229 f muscle fibres, indicating that progressive muscle wasting in the double mutant was most likely due

230 neration model for pathological fibrosis and muscle wasting in the muscular dystrophies is likely gen

231 diating the pathogenesis of cachexia-induced muscle wasting in tumor-bearing mice.

232 pression of PGC-1alpha inhibited progressive muscle wasting in TWEAK-Tg mice.

233 Muscle wasting in various catabolic conditions is, at le

234 rowth and differentiation factor-15 to cause muscle wasting in vitro was determined in C2C12 myotubes

235 he search for therapeutic targets to prevent muscle wasting, in particular sarcopenia and cachexia.

236 Treatment strategies for blocking muscle wasting include correction of metabolic acidosis,

237 Muscle wasting increases the morbidity and mortality ass

238 c muscles significantly attenuated catabolic muscle wasting induced by chronic heart failure.

239 ration in mouse muscle inhibits markedly the muscle wasting induced by fasting as well as by denervat

240 se in the skeletal muscle is associated with muscle wasting, insulin resistance and diabetes.

241 Muscle wasting is a consequence of many primary conditio

242 Cachectic muscle wasting is a frequent complication of many inflam

243 Skeletal muscle wasting is a major human morbidity, and contribut

244 Muscle wasting is associated with a number of pathophysi

245 The role of glucocorticoids in muscle wasting is complex and reflects regulation at the

246 Skeletal muscle wasting is considered the central feature of cach

247 e, understanding the molecular basis of this muscle wasting is of significant importance.

248 Skeletal muscle wasting is prevalent in many chronic diseases, ne

249 Muscle wasting is primarily mediated by the activation o

250 Contributing to the muscle wasting is resistance to growth hormone (GH).

251 Severe skeletal muscle wasting is the most debilitating symptom experien

252 The pathogenic mechanism triggering muscle wasting is unknown.

253 Cancer-induced cachexia, characterized by muscle wasting, is a lethal metabolic syndrome with unde

254 Cachexia, characterized by muscle wasting, is a major contributor to cancer-related

255 Cachexia, or muscle wasting, is a serious health threat to victims of

256 om ataxia and hypertrophic cardiomyopathy to muscle wasting, male infertility, and mental retardation

257 Cirrhosis is characterized by muscle wasting, malnutrition, and functional decline tha

258 Muscle-wasting mechanisms in cancer patients are not ful

259 s of metabolism, such as insulin resistance, muscle wasting, mitochondrial dysfunction and hyperlacta

260 06, which correlated with the progression of muscle wasting observed in DM1 patients.

261 Among these critically ill patients, muscle wasting occurred early and rapidly during the fir

262 Muscle wasting occurs in both chronic heart failure (CHF

263 Muscle wasting occurs later and results from increased p

264 and strength and dramatic resistance to the muscle wasting of cancer cachexia.

265 teral sclerosis, in whom there is neurogenic muscle wasting of varying severity.

266 statin signaling pathway is downregulated in muscle wasting or atrophying diseases, with a decrease o

267 esult in individuals who develop progressive muscle wasting, or muscular dystrophy, and premature mor

268 spinal cord die progressively, resulting in muscle wasting, paralysis, and death.

269 he activation of TWEAK-Fn14 signaling causes muscle wasting, PGC-1alpha preserves muscle mass in seve

270 nisms that link genetic mutations to diverse muscle wasting phenotypes.

271 r dystrophy (CMD) is characterized by severe muscle wasting, premature death in early childhood, and

272 Thus, it could become a marker of excessive muscle wasting, providing a method for early detection o

273 The expression and activity of muscle wasting-related transcription factors, including

274 he key cachexins that mediate cancer-induced muscle wasting remain elusive.

275 ns and myostatin increased mass or prevented muscle wasting, respectively, highlighting the potential

276 severe disorder characterized by progressive muscle wasting,respiratory and cardiac impairments, and

277 F2R activation functions to prevent skeletal muscle wasting resulting from a variety of physiological

278 ally ill patients, including the established muscle wasting 'risk factors' such as ageing, immobility

279 Muscle wasting severity parallels a decline in MuSC rege

280 tended use that include glucose intolerance, muscle wasting, skin thinning, and osteoporosis.

281 gy for treatment of diseases associated with muscle wasting such as DMD and since it uses an endogeno

282 Cachexia is a muscle-wasting syndrome that contributes significantly t

283 The mechanisms underlying the muscle wasting that accompanies CKD are not well underst

284 condition characterized by extreme skeletal muscle wasting that contributes significantly to morbidi

285 IkappaB kinase beta (MIKK), causes profound muscle wasting that resembles clinical cachexia.

286 This disease is characterized by extensive muscle wasting that results in extremely weak skeletal m

287 Cachexia is characterized by inexorable muscle wasting that significantly affects patient progno

288 strate, using in vitro and in vivo models of muscle wasting, that cachectic factors are remarkably se

289 lating IL-6 are implicated in cancer-induced muscle wasting, there is limited understanding of muscle

290 ortantly, this genetic manipulation prevents muscle wasting, thereby providing strong evidence in sup

291 iquitin ligase MuRF1 are less susceptible to muscle wasting under amino acid deprivation.

292 n of SIRT1 decreased p65K310 acetylation and muscle wasting upon starvation.

293 Burn trauma triggers hypermetabolism and muscle wasting via increased cellular protein degradatio

294 romuscular disease characterized by skeletal muscle wasting, weakness, and myotonia.

295 y, this DM1 mouse model recapitulates severe muscle wasting, which has not been reported in models in

296 ay in promoting muscle growth and inhibiting muscle wasting, which may have significant implications

297 anding the underlying mechanisms of skeletal muscle wasting will provide goals for novel treatment st

298 Skeletal muscle wasting with accompanying cachexia is a life thre

299 ors of critical illness demonstrate skeletal muscle wasting with associated functional impairment.

300 pothesized that patients who developed acute muscle wasting would show distinct patterns of change in