ライフサイエンスコーパス: mitochondrial dysfunction

1 microvascular dysfunction and cardiomyocyte/mitochondrial dysfunction).

2 nes, and subsequent epithelial disorders and mitochondrial dysfunction.

3 nfolded protein response pathway and induced mitochondrial dysfunction.

4 y the accumulation of protein aggregates and mitochondrial dysfunction.

5 of apoptotic signaling pathways triggered by mitochondrial dysfunction.

6 c setting by inhibiting oxidative stress and mitochondrial dysfunction.

7 oform and ultrastructural characteristics of mitochondrial dysfunction.

8 ondrial-LD tethering, and not from intrinsic mitochondrial dysfunction.

9 nduction of endoplasmic reticulum stress and mitochondrial dysfunction.

10 ndling and increased oxidative stress due to mitochondrial dysfunction.

11 rapeutic benefit in diseases associated with mitochondrial dysfunction.

12 treatment for human diseases associated with mitochondrial dysfunction.

13 mitochondrial ribosomal proteins and caused mitochondrial dysfunction.

14 glycerol remodeling cause Barth syndrome and mitochondrial dysfunction.

15 eby preventing cytochrome c release-mediated mitochondrial dysfunction.

16 ue is associated with replicative stress and mitochondrial dysfunction.

17 to a progressive and irreversible long term mitochondrial dysfunction.

18 nonsynonymous mutations to cause generalized mitochondrial dysfunction.

19 ies to axons, perhaps to limit the impact of mitochondrial dysfunction.

20 f heart failure, but there is no therapy for mitochondrial dysfunction.

21 ed muscle function, and exacerbated ischemic mitochondrial dysfunction.

22 ed with alterations in energy metabolism and mitochondrial dysfunction.

23 T2D is also associated with mitochondrial dysfunction.

24 mulate in the IMS of neural tissue and cause mitochondrial dysfunction.

25 its cardiotoxicity which is associated with mitochondrial dysfunction.

26 ion of VDAC1 oligomerization, apoptosis, and mitochondrial dysfunction.

27 efficient fatty acid catabolism and prevent mitochondrial dysfunction.

28 h AICAR and ALCAR improved cisplatin-induced mitochondrial dysfunction.

29 of lipids that lead to oxidative stress and mitochondrial dysfunction.

30 - and aging-related diseases associated with mitochondrial dysfunction.

31 in the absence of detectable improvements in mitochondrial dysfunction.

32 y vulnerable to neurodegeneration related to mitochondrial dysfunction.

33 hogenic mechanisms of alpha-syn mutations is mitochondrial dysfunction.

34 e secretion of proinflammatory cytokines and mitochondrial dysfunction.

35 -1 and IBM was oxidative phosphorylation and mitochondrial dysfunction.

36 peutic targets based on oxidative stress and mitochondrial dysfunction.

37 cognitive deficits observed in pathological mitochondrial dysfunction.

38 acetaldehyde and reactive oxygen species and mitochondrial dysfunctions.

39 , DNA damage (including telomere attrition), mitochondrial dysfunction, a pro-inflammatory secretory

40 rrying a mutant PSEN1(P117L) gene, exhibited mitochondrial dysfunction, accumulation of 8-oxoguanine

41 The mSTAT3-drug interaction leads to mitochondrial dysfunction, accumulation of proteotoxic S

42 sitive regulators of lifespan in response to mitochondrial dysfunction across species.

43 OPA1-elicited mitochondrial dysfunction activates an integrated stress

44 Mitochondrial dysfunction activates an unfolded protein

45 stages and provide mechanistic links between mitochondrial dysfunctions, alpha-synuclein aggregation,

46 Here, we demonstrate that mitochondrial dysfunction also disrupts the structure an

47 r a defect in the protein clearance pathway, mitochondrial dysfunction, altered RNA metabolism, impai

48 ected in Alzheimer's disease (AD) experience mitochondrial dysfunction and a bioenergetic deficit tha

49 and PAH lung pericytes and the link between mitochondrial dysfunction and aberrant endothelial-peric

50 response to cytosolic perturbations, such as mitochondrial dysfunction and aberrant ion fluxes in the

51 icantly decreased cell viability by inducing mitochondrial dysfunction and activating cell apoptosis

52 care unit patients through the promotion of mitochondrial dysfunction and activation of SMAD2/3 phos

53 previous observations that CLL cells exhibit mitochondrial dysfunction and altered lipid metabolism a

54 l dynamics plays an early and causal role in mitochondrial dysfunction and Alzheimer's disease-relate

55 Alveolar epithelial cell (AEC) mitochondrial dysfunction and apoptosis are important in

56 ndrial and plasma membrane VDAC1, leading to mitochondrial dysfunction and apoptosis induction.

57 translocates to the mitochondria to initiate mitochondrial dysfunction and apoptosis.

58 higher levels of toxic glucose metabolites, mitochondrial dysfunction and apoptosis.

59 for the study of those materials that cause mitochondrial dysfunction and apoptotic cell death.

60 l neuroprotective strategy in diseases where mitochondrial dysfunction and apoptotic pathways are inv

61 is and suggest an important role of SIRT3 in mitochondrial dysfunction and brain injury after experim

62 hondrial ceramide accumulation as a cause of mitochondrial dysfunction and brain injury after stroke.

63 VNS treatment attenuated brain mitochondrial dysfunction and cell apoptosis.

64 ted by gene expression profiles highlighting mitochondrial dysfunction and cell death pathways, with

65 participated in oxidative phosphorylation in mitochondrial dysfunction and cell death.

66 tic ischemia-reperfusion is characterized by mitochondrial dysfunction and cellular energy deficits.

67 PRDX3 protected trophoblast cells against mitochondrial dysfunction and cellular senescence induce

68 bone marrow was associated with progressive mitochondrial dysfunction and consequent exacerbation of

69 strain, which has 60% mtDNA, displays modest mitochondrial dysfunction and constitutive UPR(mt) activ

70 The potential role of age-dependent mitochondrial dysfunction and cumulative oxidative stres

71 (SPFH) domain containing protein PHB2 causes mitochondrial dysfunction and defective mitochondria-med

72 phenotypes of hereditary spastic paraplegia (mitochondrial dysfunction and defects in lipid metabolis

73 Besides alpha-synuclein aggregation, mitochondrial dysfunction and dysregulation of intracell

74 gical features in Alzheimer's brains include mitochondrial dysfunction and dystrophic neurites (DNs)

75 Mitochondrial dysfunction and energy depletion in the fa

76 sed in PMP-treated tumor cells, resulting in mitochondrial dysfunction and growth inhibition, in an m

77 such as insulin resistance, muscle wasting, mitochondrial dysfunction and hyperlactatemia.

78 eased PPAR-delta transactivation ameliorated mitochondrial dysfunction and improved cell survival of

79 Thus, correction of mitochondrial dysfunction and induction of apoptosis are

80 augmented the efficacy of MAPKi by inducing mitochondrial dysfunction and inhibiting tumor bioenerge

81 treatment reversed metabolic abnormalities, mitochondrial dysfunction and kidney pathology.

82 young mice results in non-lethal progressive mitochondrial dysfunction and loss of muscle mass.

83 hese divergent processes seem to converge in mitochondrial dysfunction and metabolic distress, which

84 lies, we observe neuronal defects related to mitochondrial dysfunction and metal homeostasis defects.

85 l permeability transition pore (MPTP) causes mitochondrial dysfunction and necrosis in acute pancreat

86 ron maintenance and reveal a novel player in mitochondrial dysfunction and neurodegeneration.

87 ation abolishes WT and mutant TDP-43-induced mitochondrial dysfunction and neuronal loss, and improve

88 Mitochondrial dysfunction and oxidative damage are commo

89 Mitochondrial dysfunction and oxidative damage with age

90 with diet-induced obesity, INT-767 prevented mitochondrial dysfunction and oxidative stress determine

91 Thus, mitochondrial dysfunction and oxidative stress do not pl

92 We found that mitochondrial dysfunction and oxidative stress trigger a

93 We sought to test whether diet-induced mitochondrial dysfunction and oxidative stress would inc

94 ragm weakness are unknown, but might include mitochondrial dysfunction and oxidative stress.

95 t skeletal muscle hyperammonaemia results in mitochondrial dysfunction and oxidative stress.

96 m of arthritis that has been associated with mitochondrial dysfunction and oxidative stress.

97 fiber atrophy and weakness in the absence of mitochondrial dysfunction and oxidative stress.

98 mdivi-1 reduced mitochondrial fragmentation, mitochondrial dysfunction and oxidative stress.

99 dynamics and quality control are involved in mitochondrial dysfunction and pathogenesis of Parkinson'

100 ous Ndufc2 knock-out rat model showed marked mitochondrial dysfunction and PBMC obtained from subject

101 ound in mitochondria, it remains unclear how mitochondrial dysfunction and protein aggregation could

102 , intracellular amyloid beta (Abeta) induces mitochondrial dysfunction and reactive oxygen species, w

103 I IFN signaling in brown adipocytes induces mitochondrial dysfunction and reduces uncoupling protein

104 of cytochrome c oxidase (COX), which led to mitochondrial dysfunction and subsequent experimental CO

105 tective, rescuing HTRA2 and PINK1-associated mitochondrial dysfunction and suggesting that TRAP1 acts

106 Mitochondrial dysfunction and synaptic damage are early

107 rs in diabetes, significantly contributes to mitochondrial dysfunction and to diabetic cardiomyopathy

108 re we show that bdh2 inactivation results in mitochondrial dysfunction and triggers their degradation

109 on of ATP production during rotenone-induced mitochondrial dysfunction and troglitazone (Rezulin)-ind

110 icient axons exhibit defects associated with mitochondrial dysfunction and we show that Tctp interact

111 ross multiple generations may involve either mitochondrial dysfunction and/or epigenetic modification

112 -3 and downregulation of p62, and aggravated mitochondrial dysfunctions and ER stress as shown by inc

113 nt animal models, we find a central role for mitochondrial dysfunction, and for impaired autophagy as

114 he production of phosphorylated Tau, reduces mitochondrial dysfunction, and maintains mitochondrial d

115 on of Drp1 reduces Abeta production, reduces mitochondrial dysfunction, and maintains mitochondrial d

116 an accumulation of reactive oxygen species, mitochondrial dysfunction, and neurodegeneration.

117 ns and stressors, impaired immune responses, mitochondrial dysfunction, and neuroinflammation.

118 ignaling signatures, CTL-mediated apoptosis, mitochondrial dysfunction, and Nrf2-modulated antioxidat

119 mineralization, cytoskeletal rearrangement, mitochondrial dysfunction, and reduced type 1 collagen s

120 mitochondrial amyloid pathology and synaptic mitochondrial dysfunction, and suppresses mitochondrial

121 s in ribosomal DNA (rDNA) transcription have mitochondrial dysfunction, and, accordingly, this is fou

122 Also, lipid peroxidation and mitochondrial dysfunction appeared to be involved in fer

123 xidative and nitrosative stress resulting in mitochondrial dysfunction are an early event in the path

124 wever, mechanisms linking lipid overload and mitochondrial dysfunction are incompletely understood.

125 Fatty liver, oxidative stress, and mitochondrial dysfunction are key pathophysiological fea

126 Genetic disorders due to mitochondrial dysfunction are not uncommon and the major

127 The toxicity of misfolded proteins and mitochondrial dysfunction are pivotal factors that promo

128 drial glutathione homeostasis and subsequent mitochondrial dysfunction are responsible for neuronal c

129 ney, and defects in fatty acid oxidation and mitochondrial dysfunction are universally involved in di

130 be consistent with observations of prominent mitochondrial dysfunction as a critical early event in t

131 Brown-Vialetto-Van Laere syndrome, implicate mitochondrial dysfunction as a downstream consequence of

132 to chemotherapeutic agents via induction of mitochondrial dysfunction as shown in in vitro and in vi

133 Thus, mutated YARS2 aggravates mitochondrial dysfunctions associated with the m.11778G>

134 In Parkinson disease (PD), mitochondrial dysfunction associates with nigral dopamin

135 ster prion strain have little or no signs of mitochondrial dysfunction at the disease midpoint but su

136 This leads to a positive feedback cycle of mitochondrial dysfunction, ATP loss, and reactive oxygen

137 tersection of the unfolded protein response, mitochondrial dysfunction, autophagy, and the innate imm

138 Cells sense and respond to mitochondrial dysfunction by activating a protective tra

139 Furthermore, sesamol treatment elicited mitochondrial dysfunction by inducing a loss of mitochon

140 -induced mitochondrial ROS generation causes mitochondrial dysfunction by inducing post-translational

141 If mitochondrial dysfunction can cause diabetes, then we hy

142 Mitochondrial dysfunction can cause female infertility.

143 SB in a neuroblastoma cell line converges on mitochondrial dysfunction caused by defects in ribosomal

144 Mitochondrial dysfunction caused pancreatic ER stress, i

145 Our data demonstrated that mitochondrial dysfunctions caused by the m.7551A > G mut

146 Mitochondrial dysfunction connects metabolic disturbance

147 evidence indicates that oxidative damage and mitochondrial dysfunction contribute to the sarcopenic p

148 ucial for mitochondrial homeostasis and that mitochondrial dysfunction contributes to altered barrier

149 Mitochondrial dysfunction contributes to APAP-induced li

150 Mitochondrial dysfunction contributes to the pathogenesi

151 RATIONALE: Vascular endothelial mitochondrial dysfunction contributes to the pathogenesi

152 blem of perturbed cholesterol metabolism and mitochondrial dysfunction could be widespread in neurolo

153 ortantly, cross-talk between IL-4, ADMA, and mitochondrial dysfunction could explain how obesity and

154 nduced ischemic limb necrosis, myopathy, and mitochondrial dysfunction, despite no improvement in lim

155 onse to acute stress induced by doxorubicin, mitochondrial dysfunction develops in the heart, trigger

156 links extracellular inflammatory signals to mitochondrial dysfunction during AKI partly via PPARGC1A

157 We show skeletal muscle mitochondrial dysfunction during hyperammonaemia in a co

158 utions of each of the toxicity mechanisms to mitochondrial dysfunction during the acute and chronic s

159 rm the transitory (mTBI) or permanent (sTBI) mitochondrial dysfunction, enhancing MQC importance to m

160 Mitochondrial dysfunction entailing decreased energy-tra

161 cient ferredoxin NADP reductase activity and mitochondrial dysfunction evidenced by low oxygen consum

162 Mitochondrial dysfunction, fragmentation and impaired tr

163 NA) inhibition of Drp-1 reversed BPA-induced mitochondrial dysfunctions, fragmentation, and apoptosis

164 show that 1 enters CSC mitochondria, induces mitochondrial dysfunction, generates reactive oxygen spe

165 Although mitochondrial dysfunction has become an established hall

166 Although mitochondrial dysfunction has been associated with dendr

167 Mitochondrial dysfunction has been linked to both cellul

168 Although mitochondrial dysfunction has been linked to the deregul

169 Mitochondrial dysfunction has long been implicated in PD

170 Mitochondrial dysfunction has previously been implicated

171 Inflammation, lipotoxicity and mitochondrial dysfunction have been implicated in the pa

172 eviates, respectively, high-fat diet-induced mitochondrial dysfunction, hepatosteatosis, and insulin

173 hyperglycemia damage DRG neurons and induce mitochondrial dysfunction; however, the impact of free f

174 with abnormal increases in cytosolic Ca(2+), mitochondrial dysfunction, impaired autophagy, and endop

175 tion/oxidative stress, increased senescence, mitochondrial dysfunction, impaired proteostasis and red

176 -insulin resistant rats by attenuating brain mitochondrial dysfunction, improving brain insulin sensi

177 deficiency, and their inactivation enhances mitochondrial dysfunction in a glutaminolysis-dependent

178 tion of ribosomal DNA transcription leads to mitochondrial dysfunction in a number of cell lines.

179 Here, we review the role of mitochondrial dysfunction in acute and chronic degenerat

180 marizes preclinical and clinical evidence of mitochondrial dysfunction in AKI and CKD.

181 In vivo evidence for brain mitochondrial dysfunction in animal models of Huntington

182 These results suggest a pivotal role for mitochondrial dysfunction in APOL1-associated kidney dis

183 al functional implications between Smads and mitochondrial dysfunction in cancer and metabolic and ne

184 displayed gene expression patterns linked to mitochondrial dysfunction in HEK293 Tet-on APOL1 cell pa

185 sent work provides a better understanding of mitochondrial dysfunction in Huntington's disease (HD) b

186 Mitochondrial dysfunction in kidney cells has been impli

187 These findings provide a novel mechanism for mitochondrial dysfunction in lipotoxic cardiomyopathy.

188 owing body of evidence suggests multifaceted mitochondrial dysfunction in mental disorders, which is

189 Mitochondrial dysfunction in pancreas of mice with AP wa

190 e results suggest that TFV and ADV may cause mitochondrial dysfunction in renal tubular cells and rep

191 trongly suggest that E50K is associated with mitochondrial dysfunction in RGC degeneration in synergy

192 ribution in the pyramidal neurons along with mitochondrial dysfunction in the brain of Alzheimer's di

193 tion factors alters CL metabolism and causes mitochondrial dysfunction in the cells.

194 has remained elusive, recent work implicates mitochondrial dysfunction in the disease progression.

195 mPTP to bridge cytosolic stress signal with mitochondrial dysfunction in the heart.

196 aim of this study was to assess the role of mitochondrial dysfunction in the impaired immunomodulato

197 together, our results demonstrate a role for mitochondrial dysfunction in the pathogenesis of GSDIa,

198 tein has a dominant-negative effect, causing mitochondrial dysfunction in the setting of an abnormal

199 use of mitochondrial disease and age related mitochondrial dysfunction in tissues including brain and

200 PRDX3 knockdown induced oxidative stress and mitochondrial dysfunction in trophoblast cells.

201 n intracellular pools of GSH needed to limit mitochondrial dysfunction in tumor cells with elevated m

202 psies performed in the irradiated field; and mitochondrial dysfunction in two.

203 o generate energy, and studies have reported mitochondrial dysfunction in type II diabetes patients.

204 activated AMPK and overcame diabetes-induced mitochondrial dysfunction in vitro and in vivo.

205 in a robust, reductionist in vitro model of mitochondrial dysfunction in which primary mixed glial c

206 nd that SCS A-beta deficiency induces severe mitochondrial dysfunction including lowered oxidative ph

207 Mitochondrial dysfunctions including defective oxidative

208 Indeed, gene knockout of Polbeta caused mitochondrial dysfunction, including reduced membrane po

209 Interestingly, these cells exhibited mitochondrial dysfunction, indicated by reactive oxygen

210 Mitochondrial dysfunction induced by mitochondrial ionop

211 sults supported the hypothesis that neuronal mitochondrial dysfunction induced by mitochondrial p53 a

212 These processes such as autophagy, mitochondrial dysfunction, inflammation, oxidative stres

213 Mitochondrial dysfunction is a core component of the agi

214 Mitochondrial dysfunction is a hallmark of aging, and un

215 We conclude that mitochondrial dysfunction is a major cause of reversible

216 erotic substrates to reverse ammonia-induced mitochondrial dysfunction is a novel therapeutic approac

217 Mitochondrial dysfunction is a pathological mediator of

218 Because mitochondrial dysfunction is an early hallmark of hypoxi

219 Mitochondrial dysfunction is an early prominent feature

220 Mitochondrial dysfunction is associated with a spectrum

221 Because mitochondrial dysfunction is associated with many acute

222 Mitochondrial dysfunction is associated with many human

223 Mitochondrial dysfunction is associated with numerous ac

224 Mitochondrial dysfunction is at the core of many disease

225 Retrograde signaling is a mechanism by which mitochondrial dysfunction is communicated to the nucleus

226 Mitochondrial dysfunction is linked with the etiopathoge

227 Mitochondrial dysfunction is one of the major contributo

228 Mitochondrial dysfunction is pervasive in human patholog

229 hondrial respiration in the brain.IMPORTANCE Mitochondrial dysfunction is present in most major neuro

230 itochondrial functional assays revealed that mitochondrial dysfunction is reduced in APPXDrp1+/- mice

231 Mitochondrial dysfunction is the most prominent source o

232 n's disease (PD) is incompletely understood, mitochondrial dysfunction is thought to play a crucial r

233 , but how these are related to PINK1-induced mitochondrial dysfunction is unknown.

234 st evidence that defective mt:RNase P causes mitochondrial dysfunction, lethality and aberrant mitoch

235 involves a pathological triad consisting of mitochondrial dysfunction, loss of integrity of neuronal

236 treatment reduces Abeta production, reduces mitochondrial dysfunction, maintains mitochondrial dynam

237 ndings suggest that PC(O-16:0/2:0)-dependent mitochondrial dysfunction may be an underlying contribut

238 Therefore, mitochondrial dysfunction may be central to the etiology

239 ent findings provide novel insights into how mitochondrial dysfunction may cause pancreatic beta-cell

240 he results suggest that metal imbalances and mitochondrial dysfunction may contribute to defects in s

241 Age-associated mitochondrial dysfunction may contribute to vascular dis

242 s show that DKD susceptibility was linked to mitochondrial dysfunction, mediated largely by Edn1-Ednr

243 a phosphorylation as a critical regulator of mitochondrial dysfunction-mediated selective dendritic l

244 In addition, cardiomyopathies resulting from mitochondrial dysfunction, metabolic abnormalities, stor

245 rative conditions are increasingly linked to mitochondrial dysfunction, methods for studying brain ce

246 ating for the lack of ERMES, suggesting that mitochondrial dysfunction might be the basis for ChAc.

247 ction of thioredoxin, has been implicated in mitochondrial dysfunction, mitophagic dysregulation and

248 Based on the mitochondrial dysfunction observed in fibroblasts and br

249 In conclusion, intrinsic mitochondrial dysfunction observed in type 1 diabetes al

250 During sepsis and shock states, mitochondrial dysfunction occurs.

251 During mitochondrial dysfunction or the accumulation of unfolde

252 4L to CD44H cell conversion in vitro induces mitochondrial dysfunction, oxidative stress and cell dea

253 d elevation in toxic glucose metabolites and mitochondrial dysfunction, partially by increasing glyco

254 As mitochondrial dysfunction, particularly of the oxidative

255 ng the EIF2, eIF4/p70S6K, mTOR signaling and mitochondrial dysfunction pathways.

256 Mitochondrial dysfunction plays a critical role in the d

257 There is substantial evidence that mitochondrial dysfunction plays a significant role in th

258 These results suggest that mitochondrial dysfunction, possibly exacerbated by prion

259 a conserved hypoxia program characterized by mitochondrial dysfunction, proinflammatory gene activati

260 Among these, lipid metabolism and mitochondrial dysfunction proteins were overrepresented.

261 k exhibited increased atrial RyR2 oxidation, mitochondrial dysfunction, reactive oxygen species (ROS)

262 of SCA10 pathology including improvement of mitochondrial dysfunction, reduced activation of caspase

263 G2/M DNA damage checkpoint, ATM signaling, mitochondrial dysfunction, regulation of the antiviral r

264 Mitochondrial dysfunction represents a critical step dur

265 ounds protected against apoptosis-associated mitochondrial dysfunction, restoring dissipated mitochon

266 eration that promote inflammation, fibrosis, mitochondrial dysfunction, satellite cell (SC) exhaustio

267 birth suggest that the vascular endothelial mitochondrial dysfunction seen at birth in these infants

268 data highlight that, by inhibiting ANT1 and mitochondrial dysfunction, SHP2 orchestrates an intrinsi

269 red barrier structure/function downstream of mitochondrial dysfunction, Stard7 expression was knocked

270 the TNF receptor superfamily, contributes to mitochondrial dysfunction, steatosis development, and in

271 3 kinase-mTOR signaling, impaired autophagy, mitochondrial dysfunction, stem cell exhaustion, epigene

272 rapeutic strategies for conditions involving mitochondrial dysfunction, such as TBI.

273 orm these structures exacerbates preexisting mitochondrial dysfunction, suggesting that the MDC pathw

274 iR-7 against MPP(+)-induced cytotoxicity and mitochondrial dysfunction, suggesting that the protectiv

275 n-1-dependent degradation of ERK5 leading to mitochondrial dysfunction, suggesting the maintenance of

276 can cause disease states, including multiple mitochondrial dysfunctions syndrome (MMDS), sideroblasti

277 Specific signatures of mitochondrial dysfunction that are associated with disea

278 t cytokine production through GSH depletion, mitochondrial dysfunction, the activation of p62-associa

279 Mitochondrial dysfunction, the inability to efficiently

280 In cells with mitochondrial dysfunction, the potential utility of xCT

281 of the actin filament network and consequent mitochondrial dysfunction through altered Drp1 localizat

282 te new therapeutic strategies that attenuate mitochondrial dysfunction through inhibition of NIK and

283 ons for understanding the mechanisms linking mitochondrial dysfunction to disease.

284 e to adverse left ventricular remodeling and mitochondrial dysfunction to repression of distal elemen

285 as a major biochemical hub, contributions of mitochondrial dysfunction to various diseases, and sever

286 Prompted by the hypothesis that neuronal mitochondrial dysfunction underlies chemotherapy-induced

287 Despite of accumulating evidence that mitochondrial dysfunction underlies the pathogenesis of

288 the nuclear and mitochondrial genomes cause mitochondrial dysfunction via several mechanisms, includ

289 Glomerular endothelial mitochondrial dysfunction was associated with increased

290 Mitochondrial dysfunction was reduced in TauXDrp1+/- mic

291 relationship between insulin resistance and mitochondrial dysfunction, we compared mitochondrial met

292 However, more severe mitochondrial dysfunctions were observed in cell lines b

293 tudies have proposed that loss of FXN causes mitochondrial dysfunction, which triggers elevated react

294 ecific MFN2 mutations cause tissue-selective mitochondrial dysfunction with increased adipocyte proli

295 sults provide a potential genetic link among mitochondrial dysfunction with increased ectopic lipid d

296 These findings demonstrate that mitochondrial dysfunction with increased sensitivity to

297 These changes resulted in mitochondrial dysfunction with marked changes in mitocho

298 Thus, insulin resistance can lead to mitochondrial dysfunction with reduced mitochondrial siz

299 or ANAC017, demonstrating that ANAC017 links mitochondrial dysfunction with the cell wall.

300 Mitochondrial dysfunction within the brain has been obse