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

1 in tryptophan and serotonin degradation and mitochondrial dysfunction).

2 microvascular dysfunction and cardiomyocyte/mitochondrial dysfunction).

3 the increase in longevity that is induced by mitochondrial dysfunction.

4 ly associated with a profound and persisting mitochondrial dysfunction.

5 tasis to prevent excess calcium overload and mitochondrial dysfunction.

6 ct abnormalities in neuroimmune processes or mitochondrial dysfunction.

7 ncrease in FA level might be associated with mitochondrial dysfunction.

8 include complex phenotypes, mostly driven by mitochondrial dysfunction.

9 ribed that counter the fatal consequences of mitochondrial dysfunction.

10 ely linked with synaptic damage and synaptic mitochondrial dysfunction.

11 c changes associated with this Abeta-induced mitochondrial dysfunction.

12 vely in telomeres as a direct consequence of mitochondrial dysfunction.

13 levels and improves diseases associated with mitochondrial dysfunction.

14 ng from DNA repair gene dysregulation and/or mitochondrial dysfunction.

15 athway in mitophagy induction in response to mitochondrial dysfunction.

16 d mitochondrial depletion of glutathione and mitochondrial dysfunction.

17 adipocytes were cold sensitive and exhibited mitochondrial dysfunction.

18 ed fusion in a large number of diseases with mitochondrial dysfunction.

19 levels of oxidative stress, thereby inducing mitochondrial dysfunction.

20 inamide adenine dinucleotide, which leads to mitochondrial dysfunction.

21 pharmacological correction of DS-associated mitochondrial dysfunction.

22 reased mitochondrial copy number, and caused mitochondrial dysfunction.

23 in synthesis as a compensatory mechanism for mitochondrial dysfunction.

24 with mitochondria and its absence results in mitochondrial dysfunction.

25 helium and capillary endothelium and induces mitochondrial dysfunction.

26 ure of phagosome physiology with a secondary mitochondrial dysfunction.

27 ng abnormal fatty acid metabolism related to mitochondrial dysfunction.

28 in ubiquitination, antigen presentation, and mitochondrial dysfunction.

29 tabolic reprogramming that leads to platelet mitochondrial dysfunction.

30 anol and tumor necrosis factor alpha-induced mitochondrial dysfunction.

31 NAXD and to link deficient NADHX repair with mitochondrial dysfunction.

32 d that the ammonium-modified Au-NPs elicited mitochondrial dysfunction.

33 sing numbers of diseases are associated with mitochondrial dysfunction.

34 ell, but no therapies are available to treat mitochondrial dysfunction.

35 eased PAR in highly-transcribed regions, and mitochondrial dysfunction.

36 D2 expression causing an increase of ROS and mitochondrial dysfunction.

37 ath worldwide and frequently associated with mitochondrial dysfunction.

38 nes, and subsequent epithelial disorders and mitochondrial dysfunction.

39 y the accumulation of protein aggregates and mitochondrial dysfunction.

40 ed as novel pathomechanisms in diseases with mitochondrial dysfunction.

41 NAFLD has the potential to aggravate hepatic mitochondrial dysfunction.

42 previously linked to impaired glycolysis and mitochondrial dysfunction.

43 , generation of reactive oxygen species, and mitochondrial dysfunction.

44 l mitochondrial content that is reduced upon mitochondrial dysfunction.

45 no protective effect on oligomycin A-induced mitochondrial dysfunction.

46 t ~13 months of age, presumably due to overt mitochondrial dysfunction.

47 renia and bipolar disorder may be linked via mitochondrial dysfunction.

48 ation is a prominent ocular manifestation of mitochondrial dysfunction.

49 in aging yeast leads to iron limitation and mitochondrial dysfunction.

50 pathogenesis, namely inclusion formation and mitochondrial dysfunction.

51 the origins of human disorders arising from mitochondrial dysfunction.

52 and other symptoms, probably all related to mitochondrial dysfunction.

53 lowing chronic stress that are indicative of mitochondrial dysfunction.

54 beneficial outcomes in diseases that involve mitochondrial dysfunction.

55 ied by systemic and central inflammation and mitochondrial dysfunctions.

56 3) induces epigenetic alterations; 4) causes mitochondrial dysfunction; 5) induces oxidative stress;

57 xidative phosphorylation genes indicative of mitochondrial dysfunction (52% of genes in pathway).

58 Our data demonstrate that mitochondrial dysfunction, a universal feature of human

59 inflammation and oxidative stress, mitigate mitochondrial dysfunction, act as senolytics and impact

60 oxidative stress and cell function, yet how mitochondrial dysfunction affects cell activity and syna

61 acrophages from MPV17(-/-) mice, a model for mitochondrial dysfunction, also showed higher propensity

62 In this context, BRB triggered mitochondrial dysfunction and aberrant cellular energeti

63 Failure to resolve mtDNA breaks leads to mitochondrial dysfunction and affects host cells and tis

64 r neurodegenerative diseases associated with mitochondrial dysfunction and altered ER-Mito interplay.

65 ial impairment is frequently associated with mitochondrial dysfunction and altered neurotransmission.

66 neurodegenerative disorder characterized by mitochondrial dysfunction and an increase in oxidative d

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

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

69 Age-related mitochondrial dysfunction and associated oxidative stres

70 Mitochondrial dysfunction and cellular stresses activate

71 ranslation, how this process is sensitive to mitochondrial dysfunction and constantly surveyed by rib

72 ge at telomere regions that can be driven by mitochondrial dysfunction and crucially can occur indepe

73 increased cytoplasmic glycogen accumulation, mitochondrial dysfunction and disintegration, and enlarg

74 nflammation and neurodegeneration-associated mitochondrial dysfunction and dynamic abnormalities by n

75 Combined, our results demonstrate that mitochondrial dysfunction and ER stress impaired glutath

76 Perfusion bioreactors attenuated mitochondrial dysfunction and ER stress resulting in a f

77 The Cd exposure caused marked hepatic mitochondrial dysfunction and fatty acid oxidation defic

78 sults in impaired protein import, leading to mitochondrial dysfunction and focal activation of the ca

79 e culture, we found evidence that with aging mitochondrial dysfunction and IL-6 exist in a positive f

80 Hypercapnic acidosis induces mitochondrial dysfunction and impairs the ability of mes

81 ging phenotypes can be reversed by targeting mitochondrial dysfunction and implicate mitochondrial en

82 ge-dependent exacerbated features, including mitochondrial dysfunction and increased oxidative stress

83 in innate immunity, the relationship between mitochondrial dysfunction and inflammation in heart fail

84 to investigate the mechanistic link between mitochondrial dysfunction and inflammatory activation in

85 How mitochondrial dysfunction and its regulation in cancer c

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

87 Impairment of mitophagy induces mitochondrial dysfunction and lipid accumulation, thereb

88 d reveal an important new connection between mitochondrial dysfunction and lysosomal dysregulation in

89 n a possible etiologic or pathogenic role of mitochondrial dysfunction and mitochondrial DNA (mtDNA)

90 uction mediates AILI by promoting hepatocyte mitochondrial dysfunction and necrosis, and suggest that

91 lecular mechanisms that are involved in both mitochondrial dysfunction and neuroinflammation in neuro

92 ue damage, the mTOR/AKT is activated causing mitochondrial dysfunction and p15/16-dependent senescenc

93 al evidence points to an association between mitochondrial dysfunction and Parkinson's disease (PD).

94 Adiponectin deficiency induces mitochondrial dysfunction and promotes endothelial activ

95 Mitochondrial dysfunction and proteostasis failure frequ

96 ical and imaging studies and determined that mitochondrial dysfunction and reduced fatty acid oxidati

97 Loss of Pbp1 leads to mitochondrial dysfunction and reduced fitness during nut

98 PUMA deficiency suppressed APAP-induced mitochondrial dysfunction and release of cell death fact

99 inhibition exacerbated the Mito-FAP-induced mitochondrial dysfunction and sensitized cells to apopto

100 Mitochondrial dysfunction and significant changes in met

101 ystem, and its deficiency causes progressive mitochondrial dysfunction and structural abnormalities l

102 The common cause of mitochondrial dysfunction and structural changes in skel

103 Unfortunately, the ability to assess mitochondrial dysfunction and the efficacy of mitochondr

104 There is evidence that mitochondrial dysfunction and the innate immune system b

105 mechanism by which EZH2 inhibition leads to mitochondrial dysfunction and the resultant exhaustion.

106 d genes, such as SNCA, LRRK2, and CHCHD2, in mitochondrial dysfunction and their overlap with sporadi

107 bearing only m.3394T>C mutation caused mild mitochondrial dysfunctions and those harboring both m.33

108 s of function does not underlie the observed mitochondrial dysfunction, and also provides a mechanism

109 cence-associated secretory phenotype (SASP), mitochondrial dysfunction, and alterations in DNA and ch

110 active oxygen species (ROS) in the placenta, mitochondrial dysfunction, and disturbed superoxide dism

111 ls exhibited a basal elevated MitoROS level, mitochondrial dysfunction, and enhanced stress response

112 ng axonal and vascular injury, metabolic and mitochondrial dysfunction, and glial reactivity.

113 mall adipocytes, activation of immune cells, mitochondrial dysfunction, and impaired metabolism toget

114 ects, these drugs promoted oxidative stress, mitochondrial dysfunction, and insulin resistance.

115 ted that OPN blockade reversed hypertension, mitochondrial dysfunction, and kidney failure in Col4a3(

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

117 the key genes involving cell cycle control, mitochondrial dysfunction, and oxidative phosphorylation

118 crease in aortic IL-6 and Parkin, attenuated mitochondrial dysfunction, and reduced atherogenesis.

119 ce toward sympathetic dominance, and cardiac mitochondrial dysfunction, and reduced the number of act

120 reased apoptosis, oxidative stress, signs of mitochondrial dysfunction, and reduced transcription of

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

122 disrupts retinal bioenergetics resulting in mitochondrial dysfunction, and retinal degeneration and

123 d consistent enrichment in oxidative stress, mitochondrial dysfunction, and transcription initiation

124 However, the severity of mitochondrial dysfunction, and/or the specific mitochond

125 tions resulting in aberrant gene expression, mitochondrial dysfunctions, and enhanced hepatic glucone

126 es including ER stress, defective autophagy, mitochondrial dysfunction, apoptosis, inflammatory cell

127 Mitochondrial dysfunctions appear also involved in ASD p

128 r grafts have not been fully elucidated, but mitochondrial dysfunction appears to be contributory.

129 idation, mitochondrial calcium overload, and mitochondrial dysfunction are characteristics of dysfunc

130 her derailments in fatty acid metabolism and mitochondrial dysfunction are forerunners of tubular dam

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

132 We review and evaluate the evidence for mitochondrial dysfunction as a consequence of stress exp

133 Our data unveil mitochondrial dysfunction as a contributor to the impair

134 in both flies and human neurons, implicating mitochondrial dysfunction as a mechanism in biotin defic

135 response (UPR(mt)) to detect and respond to mitochondrial dysfunction as an indicator of infection.

136 Despite this, the role of mitochondrial dysfunction as an initiator, propagator, o

137 This study explores the role of mitochondrial dysfunction as an intramuscular signal for

138 In addition, TTNtv hearts showed mitochondrial dysfunction, as evidenced by decreased oxy

139 nal regulation of iron metabolism genes, and mitochondrial dysfunction, as observed in the mouse mode

140 4T>C mutation-induced alterations aggravated mitochondrial dysfunctions associated with the m.11778G>

141 ed to elevated IL (interleukin)-6 levels and mitochondrial dysfunction, associated with increased mit

142 e potential, even under conditions of severe mitochondrial dysfunction, but triggers a detrimental im

143 in the context of diabetes could accelerate mitochondrial dysfunction by disrupting protective metab

144 g mechanism was the induction of hippocampal mitochondrial dysfunction by neonatal hyperoxia.

145 Under conditions of inherent or induced mitochondrial dysfunction, cancer cells manifest overlap

146 Mitochondrial dysfunction causes Ca(2+) overload and ECM

147 rane function, endoplasmic reticulum stress, mitochondrial dysfunction, cell death, and inflammation.

148 pigenetic alterations, loss of proteostasis, mitochondrial dysfunction, cellular senescence, deregula

149 tion and regulation of cell viability, while mitochondrial dysfunction characterizes heart failure.

150 o have important implications for studies of mitochondrial dysfunction conducted in mouse models of f

151 d to determine whether mitochondrial DNA and mitochondrial dysfunction contribute to the pathogenesis

152 Mitochondrial dysfunction contributes to heart failure i

153 Mitochondrial dysfunction contributes to hypertension, b

154 Mitochondrial dysfunction could alter the redox state an

155 irment of autophagic degradation process and mitochondrial dysfunction data were confirmed in vitro u

156 Tat-Beclin1) activated mitophagy, attenuated mitochondrial dysfunction, decreased lipid accumulation,

157 in-treated pregnant rats was associated with mitochondrial dysfunction, disturbed superoxide dismutas

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

159 ific manner and is mechanistically linked to mitochondrial dysfunction, endoplasmic reticulum (ER) st

160 Upon mitochondrial dysfunction, EOL-1 is concentrated into fo

161 However, the exact pathological role of mitochondrial dysfunction, especially in mitochondrial r

162 e in potassium homeostasis, which led to the mitochondrial dysfunction followed by an acute inflammat

163 control animals, it significantly attenuated mitochondrial dysfunction following SCI.

164 A large body of evidence indicates that mitochondrial dysfunction has a major role in the pathog

165 Mitochondrial dysfunction has been associated with neuro

166 Mitochondrial dysfunction has been associated with sever

167 Mitochondrial dysfunction has been implicated in many pa

168 ected in vivo In key metabolic tissues where mitochondrial dysfunction has been implicated in T2D dev

169 s in age-related macular degeneration, where mitochondrial dysfunction has been implicated in the pat

170 Mitochondrial dysfunction has been implicated in the pat

171 Mitochondrial dysfunction has been proposed as a key eve

172 Mitochondrial dysfunction has been recognized as an esse

173 Although mitochondrial dysfunction has been suggested in RTT, les

174 Mitochondrial dysfunction has consequences not only for

175 Mitochondrial dysfunction has long been implicated in th

176 he unique and critical impact that adipocyte mitochondrial dysfunction has on increasing beta-cell ma

177 Numerous studies of mitochondrial dysfunction have been conducted using mous

178 Mechanisms of neuroimmune and mitochondrial dysfunction have been repeatedly implicate

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

180 Our results implicated oxidative stress and mitochondrial dysfunction, hormone level elevations, lip

181 MMS-induced mitochondrial dysfunction, however, is AAG-independent.

182 alpha-synuclein misfolding and aggregation, mitochondrial dysfunction, impairment of protein clearan

183 Mitochondrial dysfunction impairs muscle health and caus

184 We show that mitochondrial dysfunction impairs translational terminat

185 rcise-training programme on these aspects of mitochondrial dysfunction in a NDD-CKD cohort.For the co

186 Consistently, mTORC1 inhibition ameliorates mitochondrial dysfunction in a neuronal model of NPC.

187 viously modeled amyloid-beta (Abeta)-induced mitochondrial dysfunction in a transgenic Caenorhabditis

188 increase in oxidative stress associated with mitochondrial dysfunction in adipocytes.

189 for other studies aimed at understanding RPE mitochondrial dysfunction in aging and disease.

190 However, given the major role of mitochondrial dysfunction in AKI, there is a need to rep

191 ion data suggested the presence of extensive mitochondrial dysfunction in ATAA tissues.

192 This study is the first to assess mitochondrial dysfunction in brain and muscle in individ

193 Here, we report that mitochondrial dysfunction in Caenorhabditis elegans acti

194 cts were recognized as potential markers for mitochondrial dysfunction in conjunction with age relate

195 both sexes with genetically induced, severe mitochondrial dysfunction in DaNs (MitoPark mice), at th

196 he relationship between glucose delivery and mitochondrial dysfunction in diabetic cardiomyopathy, we

197 s triggered mitochondrial calcium influx and mitochondrial dysfunction in endothelial cells, and 12(S

198 st that CHCHD10 restoration could ameliorate mitochondrial dysfunction in FTLD-TDP.

199 ys that govern IL6 production in response to mitochondrial dysfunction in GRSF1-depleted cells.

200 conclusion that mitochondrial biogenesis and mitochondrial dysfunction in LAM cells provide a novel t

201 To investigate mitochondrial dysfunction in MSA further we examined ETC

202 This study highlights mitochondrial dysfunction in MSA pathogenesis, suggests

203 icient in MSA brain tissue, thus implicating mitochondrial dysfunction in MSA.

204 loring the mechanistic role of developmental mitochondrial dysfunction in neurodevelopmental, psychia

205 ic, and clinical evidence for apoptosome and mitochondrial dysfunction in prostate cancer racial disp

206 n shown to play a critical role in mediating mitochondrial dysfunction in response to reactive oxygen

207 endoplasmic reticulum stress, autophagy, and mitochondrial dysfunction in the acinar cells are now re

208 etion of DDX5 resulted in reduced growth and mitochondrial dysfunction in the chemoresistant SCLC cel

209 ced superoxide production is associated with mitochondrial dysfunction in the kidneys of mouse models

210 mans, and the evidence supporting a role for mitochondrial dysfunction in the pathophysiology of HFpE

211 argetable pathways, whose modulation repairs mitochondrial dysfunctions in patient-derived cells and

212 letion in cells was reflected in severity of mitochondrial dysfunction, including respiratory efficie

213 vernutrition worsened excitotoxicity-induced mitochondrial dysfunction, increasing metabolic inflexib

214 We further show that NNT loss elicits mitochondrial dysfunction independent of substantial inc

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

216 norganic nitrate prevents aspects of cardiac mitochondrial dysfunction induced by hypoxia, although t

217 Conversely, mitochondrial dysfunction-induced glutathione oxidation

218 its downstream detrimental effects, such as mitochondrial dysfunction, inflammation, and fibrosis.

219 hypoxia and can result in oxidative stress, mitochondrial dysfunction, inflammation, and overactivat

220 er time course, provided that RGC death from mitochondrial dysfunction is a cell-autonomous process.

221 Mitochondrial dysfunction is a hallmark of amyloid-beta

222 nt neurological deficits is not fully known, mitochondrial dysfunction is a key component in methamph

223 Mitochondrial dysfunction is an important cause of herit

224 Primary mitochondrial dysfunction is an under-appreciated cause

225 Mitochondrial dysfunction is associated with a spectrum

226 Mitochondrial dysfunction is associated with activation

227 th high energy demand such as the heart, and mitochondrial dysfunction is associated with cardiovascu

228 Mitochondrial dysfunction is critically involved in Park

229 Therefore, our results indicate that mitochondrial dysfunction is downstream of lysosomal alk

230 Adipose tissue mitochondrial dysfunction is emerging as a key component

231 es the risk of Alzheimer's disease (AD), and mitochondrial dysfunction is implicated in both diseases

232 l of rotator cuff disease, we tested whether mitochondrial dysfunction is implicated in muscle wastin

233 Mitochondrial dysfunction is implicated in sporadic and

234 ion to amyloid-beta plaques and tau tangles, mitochondrial dysfunction is implicated in the pathology

235 a are the main source of cellular energy and mitochondrial dysfunction is implicated in the pathology

236 nction and viability of eukaryotic cells and mitochondrial dysfunction is involved in the pathogenesi

237 Mitochondrial dysfunction is involved in the pathology o

238 compared with Parkinson's disease (PD) where mitochondrial dysfunction is known to be important.

239 Enhanced RNAi triggered by mitochondrial dysfunction is necessary for the increase

240 Mitochondrial dysfunction is postulated to be central to

241 Mitochondrial aging, which results in mitochondrial dysfunction, is strongly linked to many ag

242 ating mtDNA in human blood as a biomarker of mitochondrial dysfunction, it is important to measure bo

243 , increasing insulin sensitivity, correcting mitochondrial dysfunction, ketone-based interventions, a

244 d in mice results in genomic instability and mitochondrial dysfunction, leading to a dramatic multi-s

245 p early-onset optic atrophy, severe systemic mitochondrial dysfunction leads to very early death and

246 Brain mitochondrial dysfunction limits neurologic recovery aft

247 paired insulin secretion in conjunction with mitochondrial dysfunction, loss of protection against ox

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

249 Perhaps paradoxically, certain forms of mitochondrial dysfunction may best be buffered with "sec

250 drial fitness, rather than target downstream mitochondrial dysfunction, may aid in the search for the

251 gs of this study provide novel evidence that mitochondrial dysfunction measured in peripheral blood i

252 stered to patients with primary or secondary mitochondrial dysfunction, might be due to its function

253 those involved in oxidative phosphorylation, mitochondrial dysfunction, nutrient metabolism, cardiac

254 Mitochondrial dysfunction, often based on inherited gene

255 Mitochondrial dysfunction or loss is evident in neurodeg

256 rix remodelling, transcriptional regulation, mitochondrial dysfunction, oxidative stress, calcium and

257 Although mitochondrial dysfunction plays a key role in the pathop

258 t dysbiosis, inflammation, oxidative stress, mitochondrial dysfunction, premature ageing and epigenet

259 reas, excessive intracellular calcium causes mitochondrial dysfunction, premature zymogen activation,

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

261 Our data suggest that sustained mitochondrial dysfunction, rather than atrophy alone, un

262 MYCN levels promote metabolic reprogramming, mitochondrial dysfunction, reactive-oxygen species gener

263 hanisms that impair homeostatic responses to mitochondrial dysfunction remain unclear.

264 complication of liver surgery that involves mitochondrial dysfunction resulting from mitochondrial p

265 hronic low level exposures in adults lead to mitochondrial dysfunction, severe damage to glial cells,

266 At the cellular level, mitochondrial dysfunction starts at the synapses, then i

267 3 kinase-mTOR signaling, impaired autophagy, mitochondrial dysfunction, stem cell exhaustion, epigene

268 ion of RCD1 leads to increased expression of mitochondrial dysfunction stimulon (MDS) genes regulated

269 They include mechanisms dependent on mitochondrial dysfunction such as DOX influence on the m

270 s, and mutations in BOLA3 result in multiple mitochondrial dysfunction syndrome, a fatal disorder ass

271 in the pathogenesis of the disease, multiple mitochondrial dysfunctions syndrome.

272 Reactive oxygen species (ROS), mitochondrial dysfunction, telomere shortening, genomic

273 C and m.11778G>A mutations exhibited greater mitochondrial dysfunctions than cybrids carrying only m.

274 , there was an inherent state of endothelium mitochondrial dysfunction that could contribute to endot

275 metabolite regulation, oxidative stress, and mitochondrial dysfunction that has direct implications f

276 is results in deleterious effects, including mitochondrial dysfunction, that contribute to pathophysi

277 inflammation, oxidative stress, epigenetics, mitochondrial dysfunction, the gut microbiota, tryptopha

278 diated caspase activation and contributes to mitochondrial dysfunction, thereby promoting therapeutic

279 ts impairment of mitochondrial transport and mitochondrial dysfunction through a mechanism involving

280 rders, have been shown to be associated with mitochondrial dysfunction through multiple molecular mec

281 id accumulation can promote lipotoxicity and mitochondrial dysfunction, thus triggering hepatocyte de

282 trace mechanisms linking different forms of mitochondrial dysfunction to the ISR in proliferating mo

283 spels the notion of a universal path linking mitochondrial dysfunction to the ISR, instead revealing

284 Due to their mitochondrial dysfunction, TOP1MT-KO cells become addict

285 In mammalian cells, mitochondrial dysfunction triggers the integrated stress

286 Mitochondrial dysfunction underlies many heritable disea

287 It has been proposed that mitochondrial dysfunction underlies neuronal damage, the

288 Studies suggest that mitochondrial dysfunction underlies some forms of sepsis

289 Mitochondrial dysfunction underlies the etiology of a br

290 turbation of CBS/H(2) S activity could drive mitochondrial dysfunction via mitochondrial dynamics in

291 Glomerular endothelial mitochondrial dysfunction was associated with increased

292 otypes resemble mitochondrial disorders, and mitochondrial dysfunction was first observed in ADCA-DN.

293 Mitochondrial dysfunction was highlighted as a crucial v

294 anisms underlying APOL1 risk variant-induced mitochondrial dysfunction, we generated tetracycline-ind

295 To identify pathways that modify mitochondrial dysfunction, we performed genome-wide CRIS

296 the acquisition of glycolytic phenotypes and mitochondrial dysfunction, whereas cytochrome c restorat

297 Deficiencies in such systems lead to mitochondrial dysfunction, which is a hallmark of aging

298 ablate a number of these genes and result in mitochondrial dysfunction, which is associated with bona

299 ses a severe neurodevelopmental delay due to mitochondrial dysfunction with complex I impairments and

300 inal extension), which mechanistically links mitochondrial dysfunction with proteostasis failure.