ライフサイエンスコーパス: muscle wasting

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

2 e, and reverted airway fibrosis and systemic muscle wasting.

3 nd targeting TLR4 alone effectively abrogate muscle wasting.

4 target for the development of therapies for muscle wasting.

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

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

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

8 signaling suggest novel approaches to combat muscle wasting.

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

10 t repress skeletal muscle growth and promote muscle wasting.

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

12 ation or tenotomy did not prevent subsequent muscle wasting.

13 activation of HDAC6 in mice protects against muscle wasting.

14 d to cytoplasmic CELF1 functions in skeletal muscle wasting.

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

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

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

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

19 portunities for the treatment of progressive muscle wasting.

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

21 ions that disrupt this activity cause severe muscle wasting.

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

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

24 luding p-Mef2c, which causes Hspb7-dependent muscle wasting.

25 , which is necessary and sufficient to cause muscle wasting.

26 breakdown as the driver of cancer-associated muscle wasting.

27 a class of disorders that cause progressive muscle wasting.

28 oss, while mice lacking Myoc showed enhanced muscle wasting.

29 tive function describes two major aspects of muscle wasting.

30 acterized by chronic inflammation and severe muscle wasting.

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

32 activation of the Akt pathway to counteract muscle wasting.

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

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

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

36 function in disease states characterized by muscle wasting.

37 conditions are sufficient to cause profound muscle wasting.

38 anabolic and degradative pathways preventing muscle wasting.

39 an important target for preventing skeletal muscle wasting.

40 ulation is temporally correlated with severe muscle wasting.

41 rtant therapeutic target to prevent skeletal muscle wasting.

42 ic regulators, as protective factors against muscle wasting.

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

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

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

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

47 treating sarcopenia, frailty, and secondary muscle wasting.

48 or CPTH6, spared LLC tumor-bearing mice from muscle wasting.

49 ges on cancer-induced alterations, worsening muscle wasting.

50 in skeletal muscles to combat cancer-induced muscle wasting.

51 rmine their fate in response to promoters of muscle wasting.

52 is a key mediator of cancer-induced skeletal muscle wasting.

53 knockout were resistant to LLC tumor-induced muscle wasting.

54 impairs muscle health and causes subsequent muscle wasting.

55 ed by increased glucagon, without preventing muscle wasting.

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

57 atic amino acid catabolism without affecting muscle wasting.

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

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

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

61 Muscle wasting, a cardinal feature of cancer-associated

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

63 Debilitating cancer-induced muscle wasting, a syndrome known as cachexia, is lethal.

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

65 Muscle wasting and atrophy are regulated by multiple mol

66 s of cytoskeletal proteins and contribute to muscle wasting and atrophy.

67 Muscle wasting and cachexia have long been postulated to

68 possible pharmacological approach to prevent muscle wasting and cachexia.

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

70 euromuscular disease that causes progressive muscle wasting and cardiomyopathy.

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 Muscle wasting and diminished physical performance often

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

75 nction significantly deterred cancer-induced muscle wasting and dysfunction in a preclinical model of

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

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

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

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

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

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

82 We found that host MEK activation results in muscle wasting and lipid loss, while tumor MEK activatio

83 temic wasting and cancer cachexia, including muscle wasting and lipid loss.

84 KO mice exhibited a phenotype that included muscle wasting and metabolic endotoxemia.

85 ce improves cancer plus chemotherapy-induced muscle wasting and mitochondrial alterations.

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 r protein called laminin-alpha1, ameliorates muscle wasting and paralysis in mouse models of MDC1A, d

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

93 r mitochondrial dysfunction is implicated in muscle wasting and perturbed lipid metabolism, speculati

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

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

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

97 Exogenous miR-26a suppresses muscle wasting and renal fibrosis in obstructive kidney

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

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

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

101 Oxfu administration to C26 mice exacerbated muscle wasting and triggered autophagy or mitophagy, dec

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

103 genetic disease characterized by progressive muscle wasting and weakness and premature death.

104 Less is known on pathological age-related muscle wasting and weakness termed sarcopenia, which dir

105 on mission, has demonstrated the substantial muscle wasting and weakness, along with disruption of mu

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

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

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

109 tially plays a role in ameliorating skeletal muscle wasting and weakness.

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

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

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

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

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

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

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

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

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

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

124 Skeletal muscle wasting as a direct consequence of critical illne

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

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

127 activity may have relevance to disorders of muscle wasting associated with sustained proinflammatory

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

129 exercise, prevents oxidative stress-induced muscle wasting, at least partially, by improving the ant

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

131 Skeletal muscle wasting attributed to inactivity has significant

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

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

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

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

136 .) in tumor-bearing mice not only alleviated muscle wasting, but also prolonged survival.

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

138 usly found that p300 mediates cancer-induced muscle wasting by activating C/EBPbeta, which then upreg

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 Inactivity causes muscle wasting by triggering protein degradation and may

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

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

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

145 Skeletal muscle wasting causes both morbidity and mortality of ca

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

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

148 rapeutic approach to improve regeneration in muscle wasting conditions.

149 adjunct therapy for cancer and other serious muscle wasting conditions.

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

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

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

153 ivity and its genetic deficiency exacerbates muscle wasting; conversely, sestrin overexpression suffi

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

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

159 Cachexia is a progressive muscle wasting disease that contributes to death in a wi

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

161 Duchenne muscular dystrophy (DMD) is a fatal muscle-wasting disease arising from mutations in the dys

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

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

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

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

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

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

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

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

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

171 Its dysregulation is implicated in muscle wasting diseases.

172 enous regenerative response and ameliorating muscle-wasting diseases.

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

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

175 Duchenne muscular dystrophy is a deadly muscle-wasting disorder caused by loss of dystrophin pro

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

177 inhibition improves the phenotype in several muscle wasting disorders.

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

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

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

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

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

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

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

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

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

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

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

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

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

191 ial improvement in sCr-eGFR is likely due to muscle wasting following LVAD surgery.

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

193 In these mice, muscle wasting has been ameliorated as evidenced by incr

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

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

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

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

198 agonist AVE 0991 holds promise for reducing muscle wasting in cancer.

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

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

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

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

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

204 tic strategy for adipose tissue browning and muscle wasting in CKD patients.

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

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

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

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

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

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

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

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

213 ore, the targeted deletion of PERK increases muscle wasting in Lewis lung carcinoma tumor-bearing mic

214 -mediated activation of XBP1 causes skeletal muscle wasting in LLC tumor-bearing mice.

215 get of IRE1alpha arm of the UPR, ameliorates muscle wasting in LLC tumor-bearing mice.

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

217 scriptional mechanism that mediates skeletal muscle wasting in murine models of cancer cachexia that

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

219 s miR-26 could suppresses renal fibrosis and muscle wasting in obstructive kidney disease.

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

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

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

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

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

225 of the lower limb has been shown to reverse muscle wasting in these patients but its effect on cardi

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

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

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

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

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

231 Muscle wasting increases the morbidity and mortality ass

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

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

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

235 Muscle wasting is a consequence of many primary conditio

236 Skeletal muscle wasting is a devastating consequence of cancer th

237 Cachectic muscle wasting is a frequent complication of many inflam

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

239 Skeletal muscle wasting is also common in COPD, but less is known

240 Muscle wasting is associated with increased mortality an

241 Skeletal muscle wasting is considered the central feature of cach

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

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

244 The pathogenic mechanism triggering muscle wasting is unknown.

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

246 Cancer-associated cachexia, characterized by muscle wasting, is a lethal metabolic syndrome without d

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

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

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

250 Muscle-wasting mechanisms in cancer patients are not ful

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

252 06, which correlated with the progression of muscle wasting observed in DM1 patients.

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

254 Muscle wasting occurs in both chronic heart failure (CHF

255 Muscle wasting occurs later and results from increased p

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

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

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

259 Muscle wasting, or muscle atrophy, can occur with age, i

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

261 se caused by motor neuron loss, resulting in muscle wasting, paralysis and eventual death.

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

263 Muscle wasting pathway proteins were upregulated while t

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

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

266 exercise capacity due to aging, frailty, and muscle wasting poses major unmet clinical needs.

267 eterioration in bodyweight, tachycardia, and muscle wasting, predisposing affected individuals to sub

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

269 Muscle wasting reduces functional capacity and increases

270 How sarcopenia and muscle wasting relate to such poor outcomes requires loo

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

272 dic DUX4 expression leads to the generalized muscle wasting remains unclear.

273 Here, we report cancer-induced muscle wasting requires the transcriptional cofactor p30

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

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

276 ) is a uniformly fatal condition of striated muscle wasting resulting in premature death from respira

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

278 Muscle wasting severity parallels a decline in MuSC rege

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

280 copenia, a debilitating age-related skeletal muscle wasting syndrome.

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

282 ith metastatic cancer develop a debilitating muscle-wasting syndrome, known as cachexia, that is asso

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 rom cachexia, an immune-metabolic disease of muscle wasting that impairs fitness of wild-type mice.

286 oc as a novel mechanism of cancer-associated muscle wasting that is similarly disrupted in muscle of

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

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

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

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

291 To study their role in diabetic muscle wasting, we created mice with muscle-specific tri

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

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

294 p300 is a key mediator of LLC tumor-induced muscle wasting whose acetyltransferase activity may be t

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

296 Skeletal muscle wasting with accompanying cachexia is a life thre

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

298 demonstrate coordinate induction of systemic muscle wasting with tumour-autonomous Yorkie-mediated SL

299 improved locomotor activity, and attenuated muscle wasting, with the majority of these effects depen

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