ライフサイエンスコーパス: mitophagy

1 minin through the induction of autophagy and mitophagy.

2 ondrial membrane potential and activation of mitophagy.

3 s and its knockdown reduces parkin-dependent mitophagy.

4 nt of phagophore biogenesis in xenophagy and mitophagy.

5 vascular mitochondrial function and impaired mitophagy.

6 tic ablation of ANT paradoxically suppresses mitophagy.

7 mTORC2 activation and suppresses UVB-induced mitophagy.

8 rients may eliminate mtDNA mutations through mitophagy.

9 ss of mitochondria-lysosome interplay during mitophagy.

10 ogate binding to TIM44 and TIM23 and inhibit mitophagy.

11 required to enhance its binding to Ub during mitophagy.

12 and blocks the induction of PINK-1-mediated mitophagy.

13 utophagic removal of damaged mitochondria by mitophagy.

14 respondingly, inhibition of MYCN reactivated mitophagy.

15 creased or decreased its tendency to undergo mitophagy.

16 y a few proteins are known to participate in mitophagy.

17 f mitochondrial fragmentation in Dox-induced mitophagy.

18 of MnSOD leading to mitochondrial injury and mitophagy.

19 iated by unchecked mitochondrial fission and mitophagy.

20 p1-dependent mitochondrial fragmentation and mitophagy.

21 trated by LC3-positive autophagosomes during mitophagy.

22 in mitochondria is necessary for UVB-induced mitophagy.

23 ss of mitochondrial quality control known as mitophagy.

24 nchoring protein, suppresses Parkin-mediated mitophagy.

25 pothermia are due to preserved autophagy and mitophagy.

26 Bcl2l13 knockdown in eMSCs increased mitophagy.

27 al quality through DCT-1 and ULK-1-dependent mitophagy.

28 h and effective mitochondrial degradation by mitophagy.

29 viding mitochondrial quality control through mitophagy.

30 in is an E3 ubiquitin ligase, functioning in mitophagy.

31 to damaged mitochondria and target them for mitophagy.

32 ion, enhanced membrane damage, and defective mitophagy.

33 function through regulating parkin-mediated mitophagy.

34 interfering with mitochondrial dynamics and mitophagy.

35 omain of Tollip, but independent of Tom1 and mitophagy.

36 analogous to PINK1-Parkin regulation during mitophagy.

37 tify numerous components of parkin-dependent mitophagy(1).

38 Mitophagy, a term coined to describe autophagy that targ

39 dings uncover an essential role of vIRF-1 in mitophagy activation and promotion of HHV-8 lytic replic

40 chondrial fragmentation along with excessive mitophagy activation has been detected in FECD; however,

41 Here, the role of oxidative stress in mitophagy activation in FECD is investigated.

42 andidates, revealing UMI-77 as an unexpected mitophagy activator.

43 Furthermore, HFD suppressed mitophagy activity and caused damaged mitochondria to ac

44 arized mitochondria as a result of decreased mitophagy activity and displayed functional, transcripto

45 Cardiac function, mitochondria function, and mitophagy activity were examined.

46 at attenuating this process by silencing the mitophagy adapter p62/sequestosome-1 (SQSTM1) might miti

47 protein sequestosome (p62/SQSTM1) and of the mitophagy adaptor optineurin (OPTN).

48 n without functional autophagy machinery and mitophagy adaptors.

49 With disrupted mitophagy affecting such a wide array of physiological p

50 Importantly, mitophagy after DNA damage is a vital cellular response

51 Our results indicate that modulation of mitophagy after DNA damage is independent of the type of

52 acroautophagy and selective autophagy (e.g., mitophagy, aggrephagy) can influence cellular processes,

53 egulators of canonical PINK1/parkin-mediated mitophagy, alongside noncanonical PINK1/parkin mitophagy

54 (FUNDC1), an effector of Parkin-independent mitophagy, also participates in cellular plasticity by s

55 Activation of mitophagy ameliorates mitochondrial defects and exerts a

56 Pharmacologically enhancing mitophagy and accelerating the removal of damaged mitoch

57 tion of other key signaling pathways such as mitophagy and apoptosis.

58 P1 and NIPSNAP2 have a redundant function in mitophagy and are predominantly expressed in different t

59 Mitochondrial dynamics, mitophagy and calcium uptake proteins were abundant duri

60 b9 at serine 179 is critical for alternative mitophagy and cardioprotection under energy stress condi

61 ix depletion totally abrogates Rhes-mediated mitophagy and cell death in the cultured striatal neuron

62 tophagy, to disrupt DeltaPsi (m) and promote mitophagy and cell death.

63 ntial (DeltaPsi (m) ) and promotes excessive mitophagy and cell death.

64 Mice that lack ANT1 show blunted mitophagy and consequent profound accumulation of aberra

65 Miltefosine treatment induced mitophagy and dampened NLRP3 inflammasome assembly.

66 Here we report impaired mitophagy and depletion of NAD(+), a fundamental ubiquit

67 tin ligase parkin is a critical regulator of mitophagy and has been identified as a susceptibility ge

68 n within the aorta, associated with enhanced mitophagy and increased Parkin levels.

69 hetamine combined with HIV proteins inhibits mitophagy and induces neuronal damage, and NAC reverses

70 In skeletal muscle, mitophagy and its molecular mechanisms require more thor

71 ochondria inhibits HHV-8 replication-induced mitophagy and leads to an accumulation of mitochondria.

72 rus, promoting selective types of autophagy: mitophagy and lipophagy.

73 ates PTEN-induced kinase 1 (PINK-1)-mediated mitophagy and mitochondrial accumulation of insulin rece

74 ngs suggest that enhancing Parkin-associated mitophagy and mitochondrial biogenesis after infarction

75 hondrial DNA repair, mitochondrial dynamics, mitophagy and mitochondrial biogenesis, have evolved to

76 This paralleled an increase in autophagy, mitophagy and mitochondrial biogenesis.

77 the degradation of damaged mitochondria via mitophagy and mutations in Parkin are a major cause of e

78 riatum, suggesting that Rhes is critical for mitophagy and neuronal death in vivo.

79 kin has been implicated in the regulation of mitophagy and proteasomal degradation, the precise mecha

80 ed protein, Rhes, is a critical regulator of mitophagy and striatal vulnerability in brain.

81 ther implicates inflammation due to impaired mitophagy and subsequent mtDNA release in the pathogenes

82 drial dysfunction, associated with increased mitophagy and the associated protein Parkin.

83 hat UVB-mediated MnSOD inactivation promotes mitophagy and thereby prevents accumulation of damaged m

84 ght chain 3-mediated mitochondria clearance (mitophagy) and hence facilitated the increase of mitocho

85 Specific mitochondrial autophagy (mitophagy) and mitochondrial fusion and fission are prot

86 of BRCA1) and the recycling of mitochondria (mitophagy), and peroxisomes (pexophagy).

87 hagy receptor that can be targeted to induce mitophagy, and identify MCL-1 as a drug target for thera

88 chondria fission, enhanced receptor-mediated mitophagy, and increased EC death.

89 d aberrant mitochondrial activity, decreased mitophagy, and increased lipid peroxidation.

90 impaired mitochondria respiration, defective mitophagy, and metabolic inflexibility.

91 ) dysregulates mitochondrial fission-fusion, mitophagy, and mitochondrial biogenesis.

92 reactive oxygen species (ROS), downregulated mitophagy, and poor prognosis.

93 , unfolded protein response, macroautophagy, mitophagy, and telomere maintenance) result in diverse c

94 iated by impaired mitochondrial function and mitophagy, and that bolstering cellular NAD(+) levels co

95 ochondrial deficits and specifically reduced mitophagy are evident in both sporadic and familial PD.

96 ese results suggest that autophagic flux and mitophagy are important mechanisms implicated in cardiom

97 elective autophagy pathways of xenophagy and mitophagy are initiated when the adaptor NDP52 recruits

98 Autophagy and mitophagy are probably involved in the myocardial adapta

99 Mitochondrial fission and mitophagy are quality control mechanisms that normally h

100 was increased after 3 weeks of HFD feeding (mitophagy area: 8.3% per cell with normal diet and 12.4%

101 he tumor microenvironment as well as utilize mitophagy as a survival signal is still not well underst

102 We also examine the role of mitophagy as a therapeutic target, highlighting how nutr

103 rability that is targetable to induce lethal mitophagy as an anti-tumor therapy.

104 n knockout mice, implicating Parkin-mediated mitophagy as part of its mechanism of action.

105 e oxygen species (ROS) burden and diminished mitophagy, as compared to chondrocytes from WT animals.

106 Mitophagy-associated proteins were sequentially recruite

107 We highlight mitophagy/autophagy, dopamine metabolism and the adaptiv

108 PACRG did not play a role in mitophagy but did play a role in tumor necrosis factor (

109 egulate turnover of damaged mitochondria via mitophagy, but our mechanistic understanding in neurons

110 al mechanisms have been proposed to regulate mitophagy, but these have mostly been studied using stab

111 Thus, AMPK activation promotes mitophagy by enhancing mitochondrial fission (via MFF ph

112 ission via phosphorylation of MFF and induce mitophagy by ~20%.

113 A series of experiments confirmed that mitophagy can be faithfully and quantitatively measured

114 s increasing evidence that inducing neuronal mitophagy can be used as a therapeutic intervention for

115 rbated by anomalies in PINK1/Parkin-mediated mitophagy, causing the accumulation of dysfunctional mit

116 Functions of PGAM5 include regulation of mitophagy, cell death, metabolism and aging.

117 In line with our findings in vitro, these mitophagy-compromised mice displayed reduced spontaneous

118 rstanding how dysfunctional mitochondria and mitophagy contribute to cell survival and death in BD is

119 echanism in eukaryotic cells, and defects in mitophagy correlate with aging phenomena and neurodegene

120 s, a deeper understanding of how to modulate mitophagy could provide avenues for numerous therapies.

121 ed muscle wasting and triggered autophagy or mitophagy, decreased protein synthesis, and induced mito

122 PRKN mutations, in particular in relation to mitophagy dependent disease phenotypes and provide avenu

123 Also unknown is whether mitophagy depends on pre-existing membranes or is trigge

124 Mitophagy diminishes insoluble Abeta(1-42) and Abeta(1-4

125 To measure mitophagy directly, we generated a stable skeletal muscl

126 Knockdown of Spata18 suppresses mitophagy, disturbs mitochondrial Ca2+ homeostasis, affe

127 Surprisingly, autoubiquitination and mitophagy do not appear to be required for such loss.

128 Knockdown of parkin, a positive regulator of mitophagy, dramatically diminished Dox-induced cell deat

129 p1 and PINK1 are sequestered and degraded by mitophagy during degenerative loss of post-mitotic cells

130 mary MMUT deficiency, diseased mitochondria, mitophagy dysfunction and epithelial stress, and provide

131 Mitophagy enhancement abolishes AD-related tau hyperphos

132 scovery and consider intervention points for mitophagy enhancement.

133 Mitophagy, evaluated with Mito-Keima, was increased afte

134 The localization of these mitophagy events had a robust somal bias.

135 the genetic evidence supporting the role for mitophagy failure as a pathogenic mechanism in PD.

136 pool is maintained by biogenesis, transport, mitophagy, fission, and fusion, but how these events are

137 In addition, Dox accelerated mitophagy flux, which was attenuated by DRP1 knockdown,

138 ely culminating in disturbances of autophagy/mitophagy fluxes and increased apoptosis.

139 ndently of its previously identified role in mitophagy, FUNDC1 enabled LonP1 proteostasis, which in t

140 ns, deletion of AMPK or of key autophagy and mitophagy genes normalizes the axonal mitochondrial cont

141 on of ANT-mediated ADP/ATP exchange promotes mitophagy, genetic ablation of ANT paradoxically suppres

142 Mitophagy has a pivotal role in cell homeostasis, but it

143 Mitophagy has been implicated in mitochondrial quality c

144 Research in mitophagy has boomed in recent years, and it is becoming

145 he clearance of damaged or old mitochondria (mitophagy), here we developed a high-content imaging-bas

146 rkin has been reported previously to control mitophagy, here we show that, surprisingly, parkin is di

147 We also observed that mitophagy (i.e., selective autophagic degradation of mit

148 ature of the overlapping pathways regulating mitophagy illustrate mitophagy's essential role in maint

149 These findings suggest that p53-induced mitophagy in aged white adipocytes impedes WAT beiging a

150 Importantly, enhancing mitophagy in aged, hyperlipidemic mice via oral administ

151 rter protein is dynamically regulated during mitophagy in an Aup1-dependent manner.

152 ulin blocked basal levels of PINK-1-mediated mitophagy in bronchial epithelial cells, mitochondrial t

153 that Ucp2 deletion also increased levels of mitophagy in cell culture and retinal tissue.

154 is an essential and fundamental mediator of mitophagy in health and disease.

155 ion with IFN-gamma inhibited PINK1-dependent mitophagy in macrophages through a STAT1-dependent activ

156 Assessment of mitophagy in mt-Keima Drosophila revealed an essential r

157 udy highlights the role of N-Myc in blocking mitophagy in neuroblastoma and in conferring protection

158 rifying selection against mtDNA deletions by mitophagy in postmitotic muscle fibers.

159 dergo dynamic fusion/fission, biogenesis and mitophagy in response to stimuli or stresses.

160 e translocator (ANT) complex is required for mitophagy in several cell types.

161 hat knocking-down IRGM inhibits CCCP induced mitophagy in SH-SY5Y cells.

162 Here we demonstrate that simvastatin induces mitophagy in skeletal muscle cells and hypothesized that

163 This inhibition of mitophagy in the face of statin challenge correlated wit

164 Finally, we found that UMI-77 can induce mitophagy in vivo and that it effectively reverses molec

165 in pathway is essential for the induction of mitophagy in vivo in response to hypoxic exposure and ro

166 standing the role and molecular mechanism of mitophagy in vivo.

167 ma Drosophila to extend our efforts to study mitophagy in vivo.

168 ncer cells regulate mitochondrial autophagy (mitophagy) in the tumor microenvironment as well as util

169 tophagy, alongside noncanonical PINK1/parkin mitophagy, in response to mitochondrial damage.

170 Deletion of Parkin partially inhibited mitophagy, increased lipid accumulation and exacerbated

171 Deletion of atg7 impaired mitophagy, increased lipid accumulation, exacerbated dia

172 Our results show that mitophagy increases after DNA damage in primary fibrobla

173 at sub-lethal doses, UMI-77 potently induces mitophagy, independent of apoptosis.

174 Notably, ANT promotes mitophagy independently of its nucleotide translocase ca

175 tion in fragmented mitochondria resulting in mitophagy-induced mitochondrial clearance, albeit possib

176 Treatment of AGS cells with a mitophagy inducer, carbonyl cyanide 3-chlorophenylhydraz

177 ntial therapies including NAD(+) precursors, mitophagy inducers and inhibitors of cellular senescence

178 Impairment of mitophagy induces mitochondrial dysfunction and lipid ac

179 ssential role of the PINK1-Parkin pathway in mitophagy induction in response to mitochondrial dysfunc

180 ssential role of the PINK1-Parkin pathway in mitophagy induction in vivo.

181 mary rat hippocampal neurons, we developed a mitophagy induction paradigm where mild oxidative stress

182 (ROS) within ISCs, which was associated with mitophagy induction.

183 logical interruption of vIRF-1/NIX-activated mitophagy inhibits HHV-8 productive replication.

184 s required for shaping Atg32 into functional mitophagy initiation sites and for delivery of mitochond

185 ear how Atg11 concentrates Atg32 to generate mitophagy initiation sites.

186 uncta that are thought to represent sites of mitophagy initiation.

187 recent years, and it is becoming clear that mitophagy is a complex and multi-factorial cellular resp

188 Mitophagy is a key process regulating mitochondrial qual

189 his work demonstrates that the inhibition of mitophagy is a physiological mechanism that contributes

190 Mitophagy is an evolutionarily conserved process involvi

191 Our findings demonstrate that mitophagy is an important mechanism to resist statin-ind

192 Mitophagy is an important quality-control mechanism in e

193 e decreased, mitochondria are fragmented and mitophagy is decreased.

194 The capability of NDP52 to induce mitophagy is dependent on its interaction with the FIP20

195 limination of dysfunctional mitochondria via mitophagy is essential for cell survival and neuronal fu

196 Here we provide evidence that mitophagy is impaired in the hippocampus of AD patients,

197 mpaired autophagy leads to heart failure and mitophagy is important for mitigating ischemia/reperfusi

198 become oxidative phosphorylation dependent, mitophagy is severely impaired in the PRKN mutant patien

199 ever, knowledge of Parkin's functions beyond mitophagy is still limited.

200 Mitophagy is the selective autophagy of damaged mitochon

201 ght recent studies that have changed the way mitophagy is understood, from initiation through lysosom

202 rons are glycolytic early in differentiation mitophagy is unimpaired by PRKN deficiency.

203 ctional mitochondria by selective autophagy (mitophagy) is important for cellular homeostasis and pre

204 nation of mitochondria via autophagy, termed mitophagy, is an evolutionarily conserved mechanism for

205 chondrial content of PINK1, a contributor to mitophagy, is an important area of research.

206 may exacerbate the slow kinetics of neuronal mitophagy, leading to neurodegeneration.

207 addition, we found a significant increase in mitophagy levels during Drosophila embryogenesis.

208 ferent tissues revealed a variation in basal mitophagy levels in Drosophila tissues.

209 rates in the G2019S cells and also increased mitophagy levels in HS cells.

210 We also explore how mitophagy maintains mitochondrial homeostasis at the org

211 Autophagy and mitophagy markers were examined by western blot and mito

212 IS of the DCs also accumulate autophagy and mitophagy markers, even when the kinase complex mTORC1,

213 However, unchecked mitochondrial fission and mitophagy may compromise the viability of cardiomyocytes

214 he organ and system levels and how a loss of mitophagy may play a role in a diverse group of diseases

215 ion of mitochondrial turnover as revealed by mitophagy measurements and the recovery of mitochondrial

216 canonical E3 ubiquitin ligase important for mitophagy, mirrored the effects of p62/SQSTM1 silencing.

217 During stimulation for mitophagy, mitochondria-localized parkin was severely re

218 d a significant increase in autophagic flux, mitophagy, mitochondrial mass and function in the myocar

219 le mitochondrial aggregates were labeled for mitophagy, mutant MFN2 did not inhibit Parkin-mediated d

220 s review, we will discuss the known types of mitophagy observed in mammals, recent findings related t

221 These results may indicate mitophagy or an alternate route of metabolism, respectiv

222 irect interaction in a pathway distinct from mitophagy or lysosomal degradation of mitochondrial-deri

223 But, how impaired mitophagy participates in tissue-specific vulnerability

224 suggest that targeting the parkin-dependent mitophagy pathway could be an effective strategy against

225 kin recruitment and downstream events in the mitophagy pathway.

226 We assess the tractability of mitophagy pathways and prospects for drug discovery and

227 letely blocked autophagic flux and decreased mitophagy, pexophagy, xenophagy, and ribophagy.

228 ochondria reveals that PINK1/parkin-mediated mitophagy predominantly exploits mono- and short-chain p

229 bone marrow or pharmacological inhibition of mitophagy promoted macrophage activation, which favored

230 Mitophagy protects against statin-mediated skeletal musc

231 election through a process that requires the mitophagy proteins Atg1 and BNIP3.

232 indings imply that modulating network state, mitophagy rate, and copy number to slow down heteroplasm

233 oligonucleotide treatment, which normalized mitophagy rates in the G2019S cells and also increased m

234 lecting lysosomal breakdown of mitochondria, mitophagy rates were found to be decreased in fibroblast

235 RKN) in mediating mitochondrial degradation (mitophagy) reaffirmed the importance of this process in

236 chanistic studies discovered that MCL-1 is a mitophagy receptor and directly binds to LC3A.

237 hanisms of mitophagy, reveal that MCL-1 is a mitophagy receptor that can be targeted to induce mitoph

238 2-like protein 13 (Bcl2l13), a mitochondrial mitophagy receptor, as being critical for adipogenic dif

239 Moreover, vIRF-1 binds directly to a mitophagy receptor, NIX, on the mitochondria and activat

240 Selective autophagy of mitochondria, or mitophagy, refers to the specific removal and degradatio

241 ly, we investigated the role of HO-1 and the mitophagy regulator protein Parkin on APAP-induced expre

242 attributes loss-of-function mutations in key mitophagy regulators PINK1 and Parkin to early-onset PD.

243 Autophagy and mitophagy-related markers increased in banding and remai

244 lly, we found a negative correlation between mitophagy-related proteins and TSPO levels, while VDAC c

245 However, the study of in vivo mitophagy remains limited.

246 ways, the therapeutic potential of targeting mitophagy remains to be fully explored.

247 keletal muscle C2C12 cell line, expressing a mitophagy reporter construct (mCherry-green fluorescence

248 clinical proof-of-concept, including in vivo mitophagy reporter methodologies and disease models, as

249 nuated by DRP1 knockdown, as assessed by the mitophagy reporter mt-Rosella, suggesting the necessity

250 l CRISPR-Cas9 genetic screen, using multiple mitophagy reporter systems and pro-mitophagy triggers, a

251 rictor but not raptor abrogated UVB-induced mitophagy responses.

252 putative kinase 1 and blocks Parkin-mediated mitophagy, resulting in greater mitochondrial oxidative

253 Our findings shed light on the mechanisms of mitophagy, reveal that MCL-1 is a mitophagy receptor tha

254 cally, mitochondrial uncouplers that promote mitophagy reversed LPS/IFN-gamma-mediated activation of

255 ing pathways regulating mitophagy illustrate mitophagy's essential role in maintaining the health of

256 Mitophagy serves as a critical process for maintaining m

257 Mitophagy serves as an essential quality control mechani

258 t selective autophagy, and more specifically mitophagy, shows similar dynamics.

259 The mitochondrial phenotype, including mitophagy status, is highly dependent on the metabolic s

260 and tau Caenorhabditis elegans models of AD, mitophagy stimulation (through NAD(+) supplementation, u

261 ch cooperatively initiate the process called mitophagy that identifies and eliminates damaged mitocho

262 Knocking down Mitofilin rescues the loss of mitophagy that is observed in the IRGM KD cells, suggest

263 en species, it also initiates an increase in mitophagy that is ultimately neuroprotective.

264 lleagues identify an alternative pathway for mitophagy that utilizes the serine/threonine protein kin

265 hagy (which is the most well-studied form of mitophagy), the implications of defective mitophagy to n

266 and reflect on our current understanding of mitophagy, the current challenges and the future directi

267 Mitochondrial homeostasis depends on mitophagy, the programmed degradation of mitochondria.

268 protein Atg32 is the yeast SAR that mediates mitophagy, the selective autophagic capture of mitochond

269 Mitophagy, the selective removal of damaged mitochondria

270 Mitophagy, therefore, has an important contribution to c

271 red for hypoxia and oxidative stress-induced mitophagy through NFE2L2/NRF2 transactivation.

272 RGM KD cells, suggesting that IRGM regulates mitophagy through the inhibition of Mitofilin.

273 lecular insight regarding how IRGM regulates mitophagy to control the quality of mitochondria.

274 ression, and specifically, the importance of mitophagy to maintain mitochondrial integrity.

275 of mitophagy), the implications of defective mitophagy to neurodegenerative processes, and unanswered

276 al regulation and the direct contribution of mitophagy to pathologies like neurodegenerative diseases

277 the mitochondria and activates NIX-mediated mitophagy to promote mitochondrial clearance.

278 omotes mitochondrial clearance by activating mitophagy to support virus replication.

279 s requires Nix (BNIP3L), a known receptor of mitophagy, to disrupt DeltaPsi (m) and promote mitophagy

280 tion, we demonstrated that the inhibition of mitophagy triggered classical macrophage activation in a

281 f the lethal excess of ROS molecules through mitophagy, triggered by the coordinated activation of NO

282 multiple mitophagy reporter systems and pro-mitophagy triggers, and identify numerous components of

283 lized hillock autophagosome accumulation and mitophagy, ultimately resulting in reduced axonal mitoch

284 We also showed that alterations in mitophagy upon environmental and genetic perturbation ca

285 confirmed the MDP-dependent induction of ISC mitophagy upon stress in vivo.

286 We previously explored in vivo mitophagy using a transgenic mouse expressing the mitoch

287 Collectively, Rhes is a major regulator of mitophagy via Nix, which may determine striatal vulnerab

288 In critically ill patients, we showed that mitophagy was inhibited in blood monocytes of patients w

289 Enhanced basal autophagy, lipophagy and mitophagy was observed in cells treated with Miltefosine

290 ction and since TSPO itself impairs cellular mitophagy, we also investigated the changes in the TSPO-

291 ecent study identifying the role of USP30 in mitophagy, we observed USP30 to be localized to punctate

292 Mitochondrial morphology, function and mitophagy were evaluated using live cell fluorescent ima

293 Although mitochondrial dynamics and mitophagy were induced at P1-7, mitochondrial biogenesis

294 nt findings related to PINK1/Parkin-mediated mitophagy (which is the most well-studied form of mitoph

295 arkin and PINK1 deficiency leads to impaired mitophagy, which causes the release of mitochondrial DNA

296 induces local clustering of mitochondria and mitophagy, which could be a homeostatic mechanism to con

297 respond to acute DNA damage with respect to mitophagy, which is an important mitochondrial quality c

298 ol release, induced AMPK phosphorylation and mitophagy, while dampening NLRP3 inflammasome assembly a

299 ferent mitochondrial matrix proteins undergo mitophagy with very different rates but, to date, the me

300 ival mechanism of mitochondrial NIX-mediated mitophagy within the hypoxic region of glioblastoma, the