ライフサイエンスコーパス: mitochondrial function

1 .6x10(8)+/-4.5x10(7), P<0.001) and augmented mitochondrial function.

2 strated the greater dependency of B cells on mitochondrial function.

3 data by analysing glutathione metabolism and mitochondrial function.

4 ted mitochondrial calcium overload modifying mitochondrial function.

5 leads to downregulation of genes that impact mitochondrial function.

6 rial fusion, a dynamic process essential for mitochondrial function.

7 owing a direct link between angiogenesis and mitochondrial function.

8 rotein is critical for lipid homeostasis and mitochondrial function.

9 ion transport, intermediary metabolism, and mitochondrial function.

10 indirectly monitor changes of metabolism and mitochondrial function.

11 that L-OPA1 and S-OPA1 differ in maintaining mitochondrial function.

12 gene expression, accompanied by compromised mitochondrial function.

13 study of biochemical mechanisms that control mitochondrial function.

14 utophagy, proteostasis, mRNA processing, and mitochondrial function.

15 neuroendocrine signaling, inflammation, and mitochondrial function.

16 with DNA and to the severe impairment of the mitochondrial function.

17 ss ATP than controls, indicating compromised mitochondrial function.

18 Tgfbr2 also rescued P2RX7-deficient Trm cell mitochondrial function.

19 tial roles in maintaining the homeostasis of mitochondrial function.

20 and IDH2 that encode proteins necessary for mitochondrial function.

21 cose and diabetes, were in genes involved in mitochondrial function.

22 s spectrometry, and assays of lymphocyte and mitochondrial function.

23 therogenesis - in particular, the effects on mitochondrial function.

24 ulfur (Fe-S) cluster biosynthesis and proper mitochondrial function.

25 e (UPR), and we hypothesized this may affect mitochondrial function.

26 represses key genes required for mitosis and mitochondrial function.

27 einuria-induced tubular damage by modulating mitochondrial function.

28 ypoxia resistance, a response that relies on mitochondrial function.

29 ereas male-biased genes were associated with mitochondrial function.

30 ellular models of toxicity via regulation of mitochondrial function.

31 mptic placenta may be prevented by improving mitochondrial function.

32 egulator of hair cell survival and essential mitochondrial function.

33 pathways including p53, DNA repair, WNT and mitochondrial function.

34 brain regions likely contributed to altered mitochondrial function.

35 uscle PCr t(1/2) at 2 weeks, implying better mitochondrial function.

36 e that dictates longevity induced by reduced mitochondrial function.

37 probably caused in part by early defects in mitochondrial function.

38 generative conditions result from defects in mitochondrial function.

39 jects with schizophrenia are associated with mitochondrial function.

40 raint-stress did not significantly influence mitochondrial function.

41 dated by using an array of assays to monitor mitochondrial function.

42 on of Psd1 is lethal in mice and compromises mitochondrial function.

43 lung mucosal barrier is dependent on proper mitochondrial function.

44 -induced myotoxicity have reported disrupted mitochondrial function.

45 tential (DeltaPsim) is a global indicator of mitochondrial function.

46 (2) S was shown to attenuate ROS and improve mitochondrial function.

47 moeostasis, cellular metabolic pathways, and mitochondrial function.

48 hemicals previously identified as increasing mitochondrial function.

49 ng to key metabolic regulators and repairing mitochondrial function.

50 In addition, DJ-1 has roles in regulating mitochondrial function.

51 hi were enriched in TAC3 and associated with mitochondrial function.

52 by positively regulating IL-2R signaling and mitochondrial function.

53 ury responses, axon survival and even axonal mitochondrial function.

54 lated genes, disrupting both carboxylase and mitochondrial function.

55 1 in regulating myogenic differentiation and mitochondrial function.

56 d acetyl-L-carnitine treatments, which boost mitochondrial function.

57 ntalizes the organelle, which is crucial for mitochondrial function.

58 plication as certain cancers rely heavily on mitochondrial functions.

59 cantly enriched in osteoblast, neuronal, and mitochondrial functions.

60 srupt critical cellular processes, including mitochondrial functions.

61 gulating the expression of genes involved in mitochondrial functions.

62 we evaluated the effects of MNRR1 levels on mitochondrial functioning.

63 mmunication, loss of proteostasis and eroded mitochondrial function(1)-these deleterious processes in

64 To determine if arginine improves mitochondrial function, 12 children with SCD-VOE (13.6 +

65 Despite the preservation of mitochondrial function, aconitase activity in T2DM heart

66 ogen sulfide (H(2)S)-a toxicant that impairs mitochondrial function-across evolutionarily independent

67 Identifying approaches to preserve mitochondrial function, adipose tissue integrity, and be

68 eration, TCA anaplerosis, redox balance, and mitochondrial function after GLS inhibition by the small

69 cells (MSC) undergo massive damage to their mitochondrial function after irradiation.

70 spine density, microglial morphology, brain mitochondrial function, Alzheimer protein, and cell deat

71 -invasive consumption and release assays and mitochondrial function analysis.

72 etion in adipocytes (STAT1 (a-KO) ) enhanced mitochondrial function and accelerated tricarboxylic aci

73 ection is also significantly associated with mitochondrial function and aging in human populations.

74 ever, whether there is a direct link between mitochondrial function and angiogenesis is unknown.

75 Deficits in mitochondrial function and arborization were reversed by

76 se in PGE(2) concentrations, which augmented mitochondrial function and autophagy and decreased trans

77 s a protein phosphatase essential for proper mitochondrial function and biogenesis during the extraut

78 interaction alone is critical in inhibiting mitochondrial function and cardiac myocyte viability usi

79 Mitochondrial function and cellular energetics, through

80 ized, less understood are the alterations in mitochondrial function and cellular metabolism that are

81 of preleukemic clonal evolution, identifying mitochondrial function and chromosome stability as key p

82 our work supports a mechanistic link between mitochondrial function and common neurodegenerative prot

83 have shown that arginine therapy can improve mitochondrial function and decrease oxidative stress.

84 t and anti-inflammatory properties, improved mitochondrial function and decreased cellular oxidative

85 oidism resulted in significant reductions in mitochondrial function and density in skeletal muscle be

86 Evidence of altered mitochondrial function and DNA damage was also found in

87 on of many genes including genes involved in mitochondrial function and electron transport.

88 e remodelled vessel at the expense of normal mitochondrial function and elevated oxidative stress wit

89 orm that permits comprehensive assessment of mitochondrial function and energy transduction.

90 ing axis that mechanistically links CBS with mitochondrial function and ER-mitochondrial tethering an

91 Skeletal muscle mitochondrial function and expression of uncoupling prot

92 Mitochondrial function and fatty acid and glucose metabo

93 ancing hepatic autophagy and in potentiating mitochondrial function and fatty acid oxidation.

94 schemic myofibers to compensate for impaired mitochondrial function and high turnover rate.

95 r results indicate a role for Ubx4p in yeast mitochondrial function and highlight that mitochondrial

96 Perturbations in mitochondrial function and homeostasis are pervasive in

97 n that ageing leads to a decline in vascular mitochondrial function and impaired mitophagy.

98 ncrease in intracellular Ca(2+), by altering mitochondrial function and impairing beta-cell identity,

99 -1alpha pathway enhance host epithelial cell mitochondrial function and improve the epithelial innate

100 , muscle biopsies, and assessment of ex vivo mitochondrial function and in vivo energy metabolism.

101 Hyperlipidemia further reduced mitochondrial function and increased the levels of Parki

102 cle mass, whereby it acts to maintain muscle mitochondrial function and limit autophagy.

103 em could help identify mechanisms regulating mitochondrial function and lipogenesis, with potential i

104 Disruption of these mechanisms affect mitochondrial function and localization to synapses as w

105 dicated that MCAT plays an essential role in mitochondrial function and maintenance of RGC axons, whi

106 ects TEC, organs, and the host by preserving mitochondrial function and metabolic fitness likely thro

107 for cell death, cell cycle, immune response, mitochondrial function and metabolic stress were signifi

108 We examine daily changing patterns of mitochondrial function and metabolism in Drosophila in v

109 r environment through coordinated changes in mitochondrial function and metabolism.

110 elerated aging in WS is mediated by impaired mitochondrial function and mitophagy, and that bolsterin

111 on, histology, use of alternative fuels, and mitochondrial function and morphology are unclear.

112 Furthermore, PA normalized Treg cell mitochondrial function and morphology in MS.

113 These changes correlate with changes in mitochondrial function and morphology; resulting in lowe

114 henotypes are associated with differences in mitochondrial function and nuclear DNA (nDNA) gene expre

115 mitochondrial morphology that impacted both mitochondrial function and physiologic rates.

116 ion end-products would induce limitations to mitochondrial function and proliferative capacity in ten

117 for JAG1 in cell survival, genes involved in mitochondrial function and protein synthesis were downre

118 Drosophila reveal an intriguing link between mitochondrial function and proteostasis.

119 ne density, microglial morphology, and brain mitochondrial function and reduced hyperphosphorylated T

120 long with restored Irp1 expression, improved mitochondrial function and reduced oxidative stress in s

121 set of FRDA in mice associated with improved mitochondrial function and reduced oxidative stress.

122 terized by progressive muscle loss, impaired mitochondrial function and reductions in the slow oxidat

123 In response to VDR-knockdown mitochondrial function and related gene-set expression i

124 aluate the cause-effect relationship between mitochondrial function and sFLT1 production, a human tro

125 (TSPO) plays an important role in regulating mitochondrial function and since TSPO itself impairs cel

126 [4HNE] a byproduct of lipid peroxidation) on mitochondrial function and structure was assessed in HL1

127 Lipid peroxidation and mitochondrial function and structure were assessed in ri

128 , is reflected by dramatic rearrangements of mitochondrial function and structure.

129 , suggesting that improved redox balance and mitochondrial function and suppression of inflammation u

130 operties of this HSP70i in the disruption of mitochondrial function and the inhibition of proteostasi

131 Treatment with mPTP inhibitors rescue mitochondrial function and thermogenesis in NCLX-null BA

132 ed that JAGGED1 maintains genes critical for mitochondrial function and tissue homeostasis.

133 activated during iron deficiency to maintain mitochondrial function and to enable erythroid different

134 the progression of neuropathy by protecting mitochondrial function and transport through the formati

135 her than provide a fuel source, impair their mitochondrial function and trigger major transcriptional

136 ng enzyme, is crucial for maintaining normal mitochondrial function and vascular development.

137 in liver cells, low-level PA (LPA) increases mitochondrial functions and alleviates the injuries indu

138 age is a vital cellular response to maintain mitochondrial functions and DNA repair.

139 to mitochondria, where it controls multiple mitochondrial functions and mitonuclear communication.

140 mming in the liver, with a downregulation of mitochondrial function, and an increase in key enzymatic

141 bitor, DMX-5804, that rescues cell survival, mitochondrial function, and calcium cycling in hiPSC-CMs

142 ages involved in oxidative phosphorylation, mitochondrial function, and calcium signaling.

143 2) study the relationship among the UPR(mt), mitochondrial function, and cardiac contractile function

144 A located within mitochondria, indicative of mitochondrial function, and cell-free (cf) mtDNA linked

145 decreases axonal protein synthesis, impairs mitochondrial function, and compromises axonal viability

146 Neurons heavily rely on mitochondrial function, and deficits in brain energy met

147 ased aortic Parkin and IL-6 levels, impaired mitochondrial function, and enhanced atherogenesis.

148 matrix regulation, unfolded protein binding, mitochondrial function, and inflammatory and immune resp

149 Fibrosis, adipogenesis, oxidative stress, mitochondrial function, and insulin sensitivity were ass

150 ts transcription, interferes with immune and mitochondrial function, and is aberrantly modified post-

151 leading to mTORC1 hyperactivation, disrupted mitochondrial function, and neurodegeneration.

152 k NR supplementation on insulin sensitivity, mitochondrial function, and other metabolic health param

153 nied by altered cardiac energetics, impaired mitochondrial function, and oxidative stress.

154 mel cells and establish a link between SOCE, mitochondrial function, and redox homeostasis.

155 ial oxidative phosphorylation genes, improve mitochondrial function, and suppress CCFs and the SASP i

156 nd HepG2 cells induces glucose independence, mitochondrial function, and the acquisition of a transcr

157 rdiovascular physiology, spinal oxygenation, mitochondrial function, and tissue perfusion in EAE.

158 NA inheritance checkpoint, exhibit increased mitochondrial function, and undergo an increase in RLS a

159 ge, impairment in carbon-source utilization, mitochondrial functioning, anti-oxidative defence system

160 nbiased transcriptome analyses, and impaired mitochondrial function, arborization, synapse formation

161 sitol 3-kinase (PI3K) activation and altered mitochondrial function are hallmarks of type 2 diabetes.

162 Among the most potent regulators of mitochondrial function are the uncoupling proteins, part

163 Here, we identify levels of mitochondrial function as a determinant for ciliogenesis

164 We also discuss the role of mitochondrial function as a therapeutic target, some key

165 hough the treatment did not achieve the same mitochondrial function as in the spinal cords of sham co

166 his effect is in part caused by a decline in mitochondrial function as well as by a reduction in lyso

167 sis was likely a response to perturbation of mitochondrial function, as reflected in decreased membra

168 a) Differentiation and embryogenesis rely on mitochondrial function; (b) mitochondrial metabolites ar

169 morphology, markers of protein turnover, and mitochondrial function between the control leg (CTL) and

170 at maintains cell survival cues by promoting mitochondrial function, but also suppresses metastatic s

171 tetrapeptide, elamipretide (SS-31), improves mitochondrial function, but mechanistic details of its p

172 The restoration of mitochondrial function by ALA/ALC was accompanied by a r

173 ability transition pore opening, rejuvenates mitochondrial function by direct association with ANT1 a

174 est that Ucp2 deletion facilitates increased mitochondrial function by improving quality control.

175 colysis in response to metabolic stress, and mitochondrial function by measuring O(2) consumption rat

176 n isolated tissues and myocytes and analyzed mitochondrial function by ultrasensitive oxygraphy.

177 nificant neuroimmune response and changes in mitochondrial function, cell-signalling pathways and dev

178 ltered mitochondrial morphology, compromised mitochondrial function, changes in intracellular Ca(2+)

179 flies also produced a phenotype of impaired mitochondrial function, characterized by respiratory cha

180 orce, slower upstroke velocity, and immature mitochondrial function compared with adult cardiomyocyte

181 icotinamide riboside (NR) on skeletal muscle mitochondrial function, content and morphology.

182 anges is critical to fully understanding how mitochondrial function contributes to both normal and pa

183 gs reveal that human METTL15 is required for mitochondrial function, delineate the evolution of methy

184 Mitochondrial function depends crucially on the maintena

185 We find that primary changes in mitochondrial function, detected in fresh tissue, are pr

186 n plays a role in the urothelium controlling mitochondrial function development and regeneration.

187 heart failure, which are caused by impaired mitochondrial function due to the loss of frataxin (FXN)

188 that PTEN-induced kinase 1 (PINK1) regulates mitochondrial function, dynamics, and turnover, we hypot

189 ntified an upregulation of genes involved in mitochondrial function early in disease progression, and

190 It affects mitochondrial function, energy levels, the lipid environ

191 An increase in mitochondrial function explains the resistance of Ucp2-d

192 er grafts and to determine correlations with mitochondrial function, graft metabolic function, and gr

193 Sirtuin1 expression and activity, mitochondrial function, graft metabolic function, and gr

194 Therapeutic activation of mitochondrial function has been suggested as an effectiv

195 y control mechanisms to preserve and restore mitochondrial function have emerged as promising therape

196 cts of NR were found on insulin sensitivity, mitochondrial function, hepatic and intramyocellular lip

197 Mitochondrial function (high-resolution respirometry and

198 roblasts and muscle biopsies showed impaired mitochondrial function, higher sensitivity to metabolic

199 Therapeutics that restore healthy mitochondrial function hold promise for treatment of the

200 Importantly, improving mitochondrial function holds promise as a new therapeuti

201 the most powerful intervention for promoting mitochondrial function; however, its impact on FRDA has

202 nd NAC reverses these deleterious effects on mitochondrial function.IMPORTANCE Human and animal studi

203 We propose that increased mitochondrial function in adipose tissue is an important

204 ll RNA sequencing revealed a perturbation of mitochondrial function in all cell types in PITRM1-knock

205 gene programs involved in thermogenesis and mitochondrial function in BAT and a blunted thermogenic

206 correlate with oxidative stress and impaired mitochondrial function in both PVI and pyramidal cells.

207 developed and optimized a method to measure mitochondrial function in brain tissue biopsy punches ex

208 that A2AR stimulation maintains or enhances mitochondrial function in chondrocytes.

209 H(2)S is responsible for the suppression of mitochondrial function in DS cells.

210 We assessed differences in mitochondrial function in gluteal (gSAT) and abdominal s

211 ining in stimulating positive adaptations in mitochondrial function in gluteal and abdominal SAT depo

212 Restoring mitochondrial function in human hepatocellular carcinoma

213 thods that are currently available to assess mitochondrial function in humans, and the evidence suppo

214 Furthermore, this led to impaired mitochondrial function in mouse muscle-an observation fo

215 portance of understanding the differences in mitochondrial function in multiple SAT depots when inves

216 ole, distinct from lipogenesis, of SREBP1 on mitochondrial function in mutant KRAS NSCLC.

217 tive stress, enforce survival, and safeguard mitochondrial function in nascent CTLs.

218 Maternal diet-induced obesity alters muscle mitochondrial function in offspring without changing ins

219 effects of inorganic nitrate and nitrite on mitochondrial function in skeletal muscle.

220 reperfusion injury, cardiac metabolism, and mitochondrial function in swine models of acute myocardi

221 lecular analyses, the present study examined mitochondrial function in the distinct transport and end

222 mmary, TTNtv leads to impaired autophagy and mitochondrial function in the heart.

223 mpt knockout has only minor consequences for mitochondrial function in the mouse liver.

224 ta cells and adipocytes both rely heavily on mitochondrial function in the regulation of optimal glyc

225 s a highly adaptable platform for evaluating mitochondrial function in vivo and in single cells, with

226 g technique to assess the pathophysiology of mitochondrial function in vivo in ALS and a potential to

227 onal gene transfer to the nucleus or loss of mitochondrial functions in Lophophytum.

228 d mitochondrial DNA (mtDNA), an indicator of mitochondrial function, in frontal, parietal, and cerebe

229 SPR/Cas9 genome editing resulted in impaired mitochondrial function, increased superoxide presence, a

230 ted simultaneously with both, autophagic and mitochondrial function, independent of Abeta pathology.

231 of itaconate and its ability to impair host mitochondrial function, independent of activity on the p

232 Thus, our results show that aberrant mitochondrial function is a key component of AOA1 pathol

233 c reprogramming to compensate for defects in mitochondrial function is an early event during adaptati

234 Typically, mitochondrial function is assessed following their isola

235 On the cellular level, mitochondrial function is critical for neuronal health.

236 Although mitochondrial function is crucial for brain homeostasis,

237 Surprisingly, their mitochondrial function is diminished.

238 MATalpha1's influence on mitochondrial function is largely mediated by its effect

239 al and physiological analyses, we found that mitochondrial function is maintained in the presence of

240 Efficient mitochondrial function is required in tissues with high

241 wth in vivo We conclude that exploitation of mitochondrial functions is a general trait of tumorigene

242 Moreover, high iron cells exhibited adequate mitochondrial functioning; leading to a reduction in acc

243 learly defined but may involve reductions in mitochondrial function, mass and biogenesis.

244 Overall, the data show that mitochondrial function matures over the perinatal period

245 Mitochondrial function matures towards birth and is depe

246 The observed changes in oxidative stress and mitochondrial function may facilitate the development of

247 ng body of evidence suggesting that aberrant mitochondrial function may impact cancer risk and therap

248 Furthermore, Ces3 inhibition led to impaired mitochondrial function measured by Seahorse.

249 Of the proteins essential for mitochondrial function, more than 98% are encoded in the

250 ase Friedreich's ataxia results in decreased mitochondrial function, neurodegeneration, and cardiomyo

251 ays responsible for neurovascular integrity, mitochondrial function, neuronal structure, protein/orga

252 otential to reverse and enhance the impaired mitochondrial function observed with aging and chronic m

253 Altered mitochondrial function occurs in sickle cell disease (SC

254 ty of non-invasive techniques to investigate mitochondrial function of the CNS in vivo.

255 on in patients with HF is causally linked to mitochondrial function of the PBMCs.

256 lar compartments, uncoupling the nuclear and mitochondrial functions of FOXM1.

257 xpressed genes (DEGs) had known or predicted mitochondrial function, of which oxidative phosphorylati

258 ted these peptides for neuronal toxicity and mitochondrial function on a retinoic acid-differentiated

259 ta-cells, including glucokinase (GK) levels, mitochondrial function, or expression of genes important

260 n of these genomes should lead to decline in mitochondrial function over time, yet no such decline is

261 on (DaN)-specific gene expression, including mitochondrial functioning, protein folding and ubiquitin

262 all subunit protein 35 (TgmS35), while other mitochondrial functions remain unaffected.

263 he surrounding environment because effective mitochondrial function requires the delivery of inputs (

264 Omaveloxolone, an Nrf2 activator, improves mitochondrial function, restores redox balance, and redu

265 units and nuclear gene mutations that affect mitochondrial function result in optic neuropathies.

266 ive to other conditions, deep phenotyping of mitochondrial function revealed a surprisingly normal bi

267 Disruption of mitochondrial function selectively targets tumour cells

268 is linked to neuronal energy metabolism and mitochondrial function.SIGNIFICANCE STATEMENT All synapt

269 n basal and methamphetamine-induced synaptic mitochondrial function.SIGNIFICANCE STATEMENT Methamphet

270 We found multiple abnormalities of mitochondrial function, suggesting impairment of glutama

271 g missense variants within genes involved in mitochondrial function (TBRG4, MTPAP and LONP1), implica

272 RR1 (CHCHD2) is a bi-organellar regulator of mitochondrial function that directly activates cytochrom

273 ential role for hnRNP H in basal and dynamic mitochondrial function that informs methamphetamine-indu

274 Detailed understanding of abnormalities in mitochondrial function that occur in patients with CAD i

275 ntial vitamins and cofactors, especially for mitochondrial functions that have a bacterial ancestry.

276 of this organelle, the clinical relevance of mitochondrial function, the methods that are currently a

277 portunistic infections demonstrated impaired mitochondrial function, the mitochondrial quality in T c

278 Due to the profound effect of temperature on mitochondrial function, this study was designed to inves

279 mitochondria to spatiotemporally "turn off" mitochondrial function through PMF dissipation in tissue

280 ote mRNA export independently of splicing or mitochondrial function, thus advancing our understanding

281 against infections are directly dependent on mitochondrial functions, thus placing mitochondria centr

282 d to correct various biochemical readouts of mitochondrial function to a 'fixed' amount of mitochondr

283 ive feedback loop with the impaired vascular mitochondrial function to accelerate atherogenesis.

284 trials using agents that specifically target mitochondrial function to improve symptoms in patients w

285 dinucleotide (NAD(+)) levels that compromise mitochondrial function trigger release of DNA damaging r

286 ins and suggesting diverse means of altering mitochondrial function under stress.

287 Mitochondrial function was assessed by measuring oxygen

288 Mitochondrial function was assessed using the Seahorse X

289 Mitochondrial function was impaired in mdKO mice, but en

290 To further determine the effect of dh404 on mitochondrial function, we used human proximal tubular c

291 effect on neuronal viability, but defects of mitochondrial function were found in the pathogenic line

292 These cold-induced changes in mitochondrial function were overlaid upon the generally

293 Some of the compound effects on mitochondrial function were UCP1- or AKAP1-independent,

294 fusion of mitochondria, thereby maintaining mitochondrial function when the balance is shifted to ex

295 ch as diabetes and obesity, impair placental mitochondrial function, which affects fetal development

296 stigate the effect of TTNtv on autophagy and mitochondrial function, which are essential for maintain

297 during T cell stimulation negatively impacts mitochondrial function, which can be reversed by iron su

298 formation, location, neuronal survival, and mitochondrial function with a view to creating an in vit

299 que capability of this technique to evaluate mitochondrial function with single-cell and subcellular

300 erlipidemia, aging elevates IL-6 and impairs mitochondrial function within the aorta, associated with