ライフサイエンスコーパス: mitophagy

1 sor to autophagic mitochondrial elimination (mitophagy).

2 n of damaged mitochondria through autophagy (mitophagy).

3 ays were shown previously to be required for mitophagy.

4 a parallel increase in mitochondrial mass or mitophagy.

5 a caused accumulation of Pink1 and activated mitophagy.

6 ant response pathways, followed by increased mitophagy.

7 ndrial biogenesis and PINK-1/DCT-1-dependent mitophagy.

8 d by a specialized autophagic process called mitophagy.

9 , can restrict mitochondrial dynamics before mitophagy.

10 , FANCD2, BRCA1, and BRCA2, are required for mitophagy.

11 ochondrial reactive oxygen species (ROS) and mitophagy.

12 ion injury, due to delayed fragmentation and mitophagy.

13 ular energy deficits; these, in turn, impair mitophagy.

14 a-associated degradation and Parkin-mediated mitophagy.

15 with the PINK1/Parkin and DJ-1 mechanisms of mitophagy.

16 ersial because ROS scavengers fail to retard mitophagy.

17 ), may act in concert during mammalian sperm mitophagy.

18 lation of damaged mitochondria and defective mitophagy.

19 s in the heart, triggering MDV formation and mitophagy.

20 actor expression, mitochondrial function and mitophagy.

21 cruit autophagosomes for execution of lethal mitophagy.

22 a to the pre-autophagic pool and upregulates mitophagy.

23 ondrial network for selective elimination by mitophagy.

24 uces PINK1/PARKIN-dependent and -independent mitophagy.

25 cated in PINK1-driven and Parkin-independent mitophagy.

26 mitochondria with low membrane potential to mitophagy.

27 itochondria and trigger their degradation by mitophagy.

28 or neurons rarely displayed Parkin-dependent mitophagy.

29 a and consequently slowing the initiation of mitophagy.

30 f an affected individual exhibited increased mitophagy.

31 ysfunction and triggers their degradation by mitophagy.

32 ation-induced autophagy, which occurs during mitophagy.

33 th increased cell proliferation and enhanced mitophagy.

34 e clearance of mitochondrial proteins during mitophagy.

35 ary receptors for PINK1- and parkin-mediated mitophagy.

36 r in the disposal of damaged mitochondria by mitophagy.

37 ecreases the selectivity for DeltaOTC during mitophagy.

38 Damaged mitochondria are removed by mitophagy.

39 aired bioenergetics, increased autophagy and mitophagy.

40 mitochondria and activates Parkin to induce mitophagy.

41 tochondrial damage-induced fragmentation and mitophagy.

42 use revealed significant variations in basal mitophagy.

43 uperoxide scavenging, and a severe defect in mitophagy.

44 thanogene 2 (BAG2) as a factor that promotes mitophagy.

45 agy mediators BNIP3 and BNIP3L, and impaired mitophagy.

46 al of damaged/dysfunctional mitochondria via mitophagy.

47 xenophagy, as well as to mitochondria during mitophagy.

48 otility before activation of Parkin-mediated mitophagy.

49 vation of the PKC pathway leads to defective mitophagy.

50 ein mt-Keima in order to more readily assess mitophagy.

51 ndrial translocation of Parkin, essential in mitophagy.

52 turally protected Ser65 residues, triggering mitophagy.

53 ria and the role of mitochondrial fission in mitophagy.

54 gesting a novel Mfn2 degradation pathway via mitophagy.

55 ecreased free GFP, consistent with decreased mitophagy.

56 for the induction of Parkin/PINK1-dependent mitophagy.

57 ding to a superoxide-dependent activation of mitophagy.

58 The induction of mitophagy, a quality control process in mitochondria, pl

59 Mitophagy, a selective autophagy for eliminating damaged

60 organelle biogenesis and quality control via mitophagy, accumulation of mitochondrial DNA (mtDNA) dam

61 s, it remains unclear whether hyperactivated mitophagy affects the maintenance and differentiation of

62 Our findings indicate that mitophagy alterations can be considered a new hallmark o

63 ted ceramide synthesis, selectively inducing mitophagy and AML cell death.

64 rial fragmentation, which is associated with mitophagy and apoptosis in vitro.

65 ded from the outer membrane independently of mitophagy and apoptosis, providing a framework for mecha

66 ay capable of rapid parallel measurements of mitophagy and autophagy in mammalian cells using a singl

67 Importantly, sesamol inhibited mitophagy and autophagy through impeding the PI3K Class

68 or of poor mitochondrial health, and lead to mitophagy and cell death.

69 P significantly delayed the process of sperm mitophagy and completely prevented it when combined with

70 pinpoint a conserved mechanism of eukaryotic mitophagy and demonstrate a function of prohibitin 2 tha

71 provide direct evidence of exercise-induced mitophagy and demonstrate the importance of Ampk-Ulk1 si

72 veolar macrophages had evidence of increased mitophagy and displayed apoptosis resistance.

73 l uncoupler treatment, stimulates widespread mitophagy and effectively eliminates mitochondria.

74 tochondrion to the nucleus, VPS13 suppresses mitophagy and functions in parallel with the endoplasmic

75 Recent studies indicate that mitophagy and healthy mitochondrial function are critica

76 tochondrial fission, in midlife, facilitates mitophagy and improves both mitochondrial respiratory fu

77 on restores mitochondrial trafficking during mitophagy and improves mitochondrial respiration and glu

78 m patients with COPD also exhibited impaired mitophagy and increased cellular senescence via suborgan

79 d IL-18 secretion, suggesting that restoring mitophagy and inhibiting inflammasome activation may ser

80 oxidative metabolism, is more frequent than mitophagy and is up-regulated on the time scale of minut

81 a-derived vesicles, organelle degradation by mitophagy and macroautophagy, and in some cases transfer

82 mplex relies on ubiquitin signals to promote mitophagy and maintain mitochondrial quality control nec

83 This allows the assessment of mitophagy and mitochondrial architecture in vivo.

84 and allows unambiguous in vivo detection of mitophagy and mitochondrial morphology at single-cell re

85 ermidine feeding enhanced cardiac autophagy, mitophagy and mitochondrial respiration, and it also imp

86 tant AML cells suppressed ceramide-dependent mitophagy and prevented cell death.

87 udies implicated Parkin in the regulation of mitophagy and proteasomal degradation, the precise mecha

88 5-hydroxycholesterol increased APAP-mediated mitophagy and protected ASMase(-/-) mice and hepatocytes

89 -)Lyz2-cre) and Park2(-/-) mice had impaired mitophagy and reduced active transforming growth factor-

90 tion to the mitochondria, corrects excessive mitophagy and reduces cell death in HD mouse- and patien

91 tochondria undergo perinatal Parkin-mediated mitophagy and replacement by mature adult mitochondria.

92 bers as primary contributors to PINK1/Parkin mitophagy and starvation autophagy.

93 of Keap1-Nrf2 PPI inhibitors as inducers of mitophagy and their potential as pharmacological agents

94 icate that Atad3a suppresses Pink1-dependent mitophagy and thereby serves a key role in hematopoietic

95 he mitochondria is both sufficient to induce mitophagy and to promote cell survival.

96 ernal transmission of mitochondria relies on mitophagy and uncover a collaboration between MUL1 and P

97 utophagy, selective mitochondrial autophagy (mitophagy), and autophagic flux.

98 s the intimate connection between autophagy, mitophagy, and cardiovascular disorders.

99 tophagic stimuli, including parkin-dependent mitophagy, and cells lacking all ATG8 proteins accumulat

100 roscopy revealed mitochondrial degeneration, mitophagy, and deformed foot processes in podocytes.

101 ains on mitochondria to facilitate efficient mitophagy, and mechanistically links genes mutated in Pa

102 ysfunction, the activation of p62-associated mitophagy, and p62-TRAF6 interaction.

103 of Drp1 prevented ceramide-dependent lethal mitophagy, and reconstitution of WT-Drp1 or phospho-null

104 that CVB localizes to mitochondria, induces mitophagy, and subsequently disseminates from the cell i

105 on rates, exacerbated PINK1/Parkin-dependent mitophagy, and transcriptional upregulation of PARK2 in

106 mitochondrial unfolded protein response and mitophagy are also reviewed, with particular emphasis pl

107 ne potential is maintained and regulators of mitophagy are downregulated.

108 egulating mitochondrial dynamics, as well as mitophagy are induced by mechanical silencing and that t

109 l, physiological or pathological triggers of mitophagy are still not fully characterized.

110 rial unfolded protein response (UPR(MT)) and mitophagy, are active may predict severity and progressi

111 ive mechanisms, such as fission, fusion, and mitophagy, are induced to eliminate damaged portions or

112 Our data thus identify mitophagy as a key mechanism of HSC expansion and sugges

113 fused mitochondrial networks and the rate of mitophagy as well as decreases the selectivity for Delta

114 dynamics (fusion and fission) and clearance (mitophagy), as well.

115 rescue was suppression of Drp1-induced hyper-mitophagy, assessed as ubiquitination of mitochondrial p

116 2DM aggravates HF after MI through defective mitophagy, associated exaggerated inflammasome activatio

117 mitochondrial oxidative stress at 3-12 h and mitophagy at 6 h post-exercise in skeletal muscle.

118 FUNDC1 integrates mitochondrial fission and mitophagy at the interface of the MAM by working in conc

119 ass and Mfn2 levels, which were rescued with mitophagy blocker, bafilomycin, in FECD.

120 e importance of K6 and K63 chain linkages in mitophagy, but phosphorylation of K63 chains by PINK1 di

121 h the orchestration of selective fission and mitophagy by PINK1.

122 Here we show that the induction of mitophagy by the mitochondrial uncoupler FCCP is indepen

123 ed in familial Parkinson's disease, promotes mitophagy by ubiquitinating mitochondrial proteins for e

124 lleviates mitochondrial defects and impaired mitophagy caused by clu depletion.

125 tochondria-accumulated VCP elicits excessive mitophagy, causing neuronal cell death.

126 Moreover, the beta-cell Clec16a-Nrdp1-USP8 mitophagy complex is destabilized and dysfunctional afte

127 hese observations suggest that Akt1-mediated mitophagy contributes to alveolar macrophage apoptosis r

128 arly, we provide evidence that NIX-dependent mitophagy contributes to mitochondrial elimination durin

129 sporadic late-onset AD suggest that impaired mitophagy contributes to synaptic dysfunction and cognit

130 These results demonstrate that mitophagy controls the activities of p53 to maintain hep

131 a-deficient mice significantly 'rescued' the mitophagy defect, which resulted in restoration of the p

132 ctivated Pkc1p, rescued crd1Delta growth and mitophagy defects.

133 uced lung cellular senescence, and restoring mitophagy delays cellular senescence, which provides a p

134 alizes with mitochondria and is removed by a mitophagy-dependent manner.

135 Whether or not mitophagy depends on prior mitochondrial fragmentation b

136 pharmacological activation of p62-dependent mitophagy directly reduced RIG-I-like receptor-dependent

137 re, we found that PINK1-Mfn2-Parkin-mediated mitophagy directs this metabolic transformation in mouse

138 understanding of mitochondrial dynamics and mitophagy during aging is missing.

139 ulates the PINK1/Parkin and DJ-1 pathways of mitophagy during sepsis.

140 r study reveals the functional importance of mitophagy during the dynamic response of these cytolytic

141 iseases including diabetic retinopathy (DR), mitophagy dysregulation and NLRP3 inflammasome activatio

142 previously described E3 ubiquitin ligase and mitophagy effector, on depolarized mitochondria in neona

143 gradative ubiquitin conjugates to direct its mitophagy effectors and stabilize the Clec16a-Nrdp1-USP8

144 ion of macroautophagy, rather than selective mitophagy, ensures apoptotic progression.

145 This allows the reversion of mitophagy failure reflected in the recovery of membrane

146 with a new model that, instead of promoting mitophagy, fission protects healthy mitochondrial domain

147 porter gene to demonstrate the occurrence of mitophagy following exercise in mice, and show this is d

148 The mitophagy function of FANCC is genetically distinct from

149 Mutants of autophagy/mitophagy genes ATG8, ATG18, and ATG32 synthetically int

150 hese results demonstrated that p62-dependent mitophagy has an immunosuppressive role to innate immune

151 The deterioration of mitophagy has been hypothesized to underlie the pathogen

152 Furthermore, although elevated mitophagy has been invoked to explain low mitochondrial

153 Impairment in mitophagy has been proven in these cells due to diminish

154 Here we demonstrate that the role of ROS in mitophagy has been underappreciated as a result of the i

155 ochondrial membrane potential (DeltaPsi) and mitophagy has not been identified.

156 this notion, genetic defects in autophagy or mitophagy have been shown to exacerbate the propensity o

157 The mechanisms underlying exercise-induced mitophagy have not been fully elucidated.

158 hough the mechanism by which Parkin mediates mitophagy in a PINK1-dependent manner is becoming cleare

159 Bcl2-L-13 induces mitophagy in Atg32-deficient yeast cells.

160 and induces mitochondrial fragmentation and mitophagy in HEK293 cells.

161 Sperm mitophagy in higher mammals thus relies on a combined ac

162 log drug, in vivo, which also induced lethal mitophagy in human AML blasts with clinically relevant F

163 n microscopy) indicted accelerated autophagy/mitophagy in injured CNPase(-/-) mice.

164 how to use confocal microscopy to visualize mitophagy in living tissues obtained from mt-Keima trans

165 PHB2 is required for Parkin-induced mitophagy in mammalian cells and for the clearance of pa

166 experiments to identify novel regulators of mitophagy in mammalian cells.

167 -13) induces mitochondrial fragmentation and mitophagy in mammalian cells.

168 coding the AAA+-ATPase Atad3a hyperactivated mitophagy in mouse hematopoietic cells.

169 th some improvements in oxidative damage and mitophagy in muscles of old mice.

170 ion in the absence of Drp1, while it induces mitophagy in Parkin-deficient cells.

171 aining for LC3 and p62 indicated an impaired mitophagy in peri-infarct regions of LV in T2DM mice com

172 This is the first report to implicate mitophagy in regulation of tumour cells with high CD44 e

173 7D-Drp1), restored mitochondrial fission and mitophagy in response to crenolanib in FLT3-ITD(+) AML c

174 MDV production is up-regulated together with mitophagy in response to doxorubicin-induced mitochondri

175 gulates AML cell death by ceramide-dependent mitophagy in response to FLT3-ITD targeting.

176 ation-mediated mitochondrial degradation and mitophagy in RGC somas in vitro, it does not affect tran

177 n recruitment it was insufficient to trigger mitophagy in the absence of broader PINK1 action.

178 ssion-mediated mitochondrial degradation and mitophagy in the axons of the glial lamina of aged E50K(

179 rs highly enriched and differential zones of mitophagy in the developing heart and within specific ce

180 mutants, is sufficient to partially restore mitophagy in the setting of PARKIN knockdown, suggesting

181 stress, and apoptosis and restored autophagy/mitophagy in the tubular cells of these mice.

182 Previous methods used to detect mitophagy in vivo were cumbersome, insensitive and diffi

183 ssment of mitochondrial oxidative stress and mitophagy in vivo, and were preceded by increased phosph

184 Although Atg32 is essential for mitophagy in yeast, no Atg32 homologue has been identifi

185 maged or depolarized mitochondria occurs via mitophagy, in which damaged mitochondria are targeted fo

186 Both situations utilize mitophagy, in which mitochondria are sequestered by auto

187 ransformed keratinocytes display evidence of mitophagy, including mitochondrial fragmentation, decrea

188 ally targeting mitochondrial translation and mitophagy increases the fitness and lifespan of GMC101 w

189 uggest that Parkin affects mtDNA levels in a mitophagy-independent manner.SIGNIFICANCE STATEMENT Park

190 In addition to the chemical mitophagy inducer, overexpression of voltage-dependent a

191 demonstrated a temporally regulated role for mitophagy-inducing proteins BCL2/adenovirus E1B 19-kDa i

192 tochondrial ceramide accumulation and lethal mitophagy induction in response to FLT3-ITD targeting wa

193 ocesses, including mitochondrial biogenesis, mitophagy, inflammasome activation, cell proliferation,

194 lthough Akt1 increased TGF-beta1 expression, mitophagy inhibition in Akt1-overexpressing macrophages

195 ight into the cardiac mitochondrial dynamism-mitophagy interactome.

196 Mitophagy is a cellular process that selectively removes

197 Mitophagy is a cellular quality-control pathway, which i

198 mitochondria and subsequent Parkin-dependent mitophagy is abrogated in glucose-free medium or in the

199 Mitophagy is an autophagic response that specifically ta

200 heart under normal healthy conditions while mitophagy is comparatively less prevalent.

201 gic process via lysosomal degradation called mitophagy is critical for mitochondrial homeostasis and

202 While mitophagy is critical to pancreatic beta-cell function,

203 When mitophagy is enhanced, p53 co-localizes with mitochondri

204 Mitophagy is essential for cellular homeostasis, but how

205 However, when mitophagy is inhibited, p53 is phosphorylated at serine-

206 bioenergetics of the cardiovascular system, mitophagy is particularly important for cardiovascular h

207 In this study, we report that mitophagy is perturbed in CL-deficient yeast cells.

208 essential for cellular homeostasis, but how mitophagy is regulated is largely unknown.

209 Parkin-mediated mitophagy is reportedly either irrelevant, or a major fa

210 Defective mitophagy is thought to contribute to normal aging and t

211 e pathway that removes damaged mitochondria (mitophagy) is also compromised in AD, resulting in the a

212 rate that mitochondrial dynamics, as well as mitophagy, is affected by mechanosensing at the transcri

213 mitochondria by autophagy, a process called mitophagy, is essential for key events in development, c

214 Autophagic turnover of mitochondria, termed mitophagy, is proposed to be an essential quality-contro

215 Deregulation of mitophagy leads to an increased number of damaged mitoch

216 In conclusion, defective mitophagy leads to CS stress-induced lung cellular senes

217 Defective mitophagy linked to dysfunction in the proteins Parkin a

218 ings in this study suggest that CVB subverts mitophagy machinery to support viral dissemination in re

219 ed mitochondrial reactive oxygen species and mitophagy marker PINK1.

220 f damaged/dysfunctional mitochondria through mitophagy may play a central role in the loss of mitocho

221 speculate that this "non-selective" form of mitophagy may potentially help to counteract the build-u

222 olster mitochondrial health and/or stimulate mitophagy may therefore forestall the neurodegenerative

223 pecies expression, reduced expression of the mitophagy mediators BNIP3 and BNIP3L, and impaired mitop

224 ive phosphorylation, mitochondrial turnover (mitophagy), mitochondrial derived oxidative stress, and

225 Within the acidic lysosome (pH 4.5) after mitophagy, mt-Keima undergoes a gradual shift to longer-

226 ing the impact of mitochondrial dynamics and mitophagy on the development and progression of cardiova

227 erine-392 by PINK1, a kinase associated with mitophagy, on mitochondria and translocated into the nuc

228 macological and genetic inhibition of either mitophagy or glycolysis consistently inhibited RGC diffe

229 ctron transport, activation of biogenesis or mitophagy, or the regulation of mitochondrial fission an

230 Mitophagy orchestrates the autophagic degradation of dys

231 d with new-onset diabetes, impairs beta-cell mitophagy, oxygen consumption, and insulin secretion.

232 Suppressing the mitophagy pathway in HL-1 cardiomyocytes with either sma

233 Blocking various steps in the mitophagy pathway reduced levels of intracellular and ex

234 r is becoming clearer, the triggers for this mitophagy pathway remain elusive.

235 hondria during viral infection, a protective mitophagy pathway was induced during the contraction pha

236 Together, parkin and PINK1 regulate the mitophagy pathway, which recycles damaged mitochondria f

237 on the PTEN-induced putative kinase 1-Parkin mitophagy pathway.

238 Therefore, the "NF-kappaB-p62-mitophagy" pathway is a macrophage-intrinsic regulatory

239 ed protein (GABARAP)] and the nontraditional mitophagy pathways involving ubiquitin-proteasome system

240 mitochondrial unfolded protein response and mitophagy pathways.

241 ific autophagic elimination of mitochondria (mitophagy) plays the role of quality control for this or

242 However, if and how mitophagy proceeds within specific cellular subtypes in

243 As mitophagy proceeds, FUNDC1/calnexin association attenuat

244 In summary, developmentally controlled mitophagy promotes a metabolic switch towards glycolysis

245 opriate transportation and processing of the mitophagy protein Pink1.

246 horylation of the LIR domain of Nix enhances mitophagy receptor engagement.

247 e protein, prohibitin 2 (PHB2), as a crucial mitophagy receptor involved in targeting mitochondria fo

248 The mitophagy receptor Nix interacts with LC3/GABARAP protei

249 y PINK1 did not enhance binding to candidate mitophagy receptors optineurin (OPTN), sequestosome-1 (p

250 gh there is some functional redundancy among mitophagy receptors, efficient sequestration of damaged

251 Mitophagy receptors, including optineurin (OPTN), nuclea

252 Local hypoxia triggered expression of the mitophagy regulator BCL2/adenovirus E1B 19-kDa-interacti

253 We propose that PINK1 functions as a master mitophagy regulator by activating Parkin and DRP1 in res

254 itination is essential for the assembly of a mitophagy regulatory complex, comprised of the E3 ligase

255 such as delta-opioid receptor regulation and mitophagy, reinforce the notion that mitochondrial adapt

256 ISC/EB-specific knockdown of the mitophagy-related genes Pink1 or Parkin suppresses the a

257 However, the precise mechanisms of mitophagy remain uncertain.

258 nce of mitochondrial damage and induction of mitophagy remains unclear.

259 m-chlorophenylhydrazone, which activates the mitophagy response, sorafenib treatment triggers PINK1/P

260 t results in small mitochondria that trigger mitophagy, resulting in a reduction in mitochondrial con

261 ese data indicate constitutive activation of mitophagy results in reduction of mitochondrial mass and

262 hoS65-ubiquitin (pUb), which constitutes the mitophagy signal.

263 is or a specialized type of autophagy termed mitophagy, SLC25A46 degradation operates independently o

264 nally truncated forms, blocking Nix-mediated mitophagy stabilizes full-length MAVS, which aggregates

265 To our surprise, we found that mitophagy still occurred in Parkin knock-out (KO) mice a

266 phatases prevented TFEB translocation during mitophagy, suggesting cross talk between these two MiT/T

267 utations in OPTN and TBK1 can interfere with mitophagy, suggesting that inefficient turnover of damag

268 itochondrial fusion, fission, biogenesis and mitophagy that determine mitochondrial morphology, quali

269 Consequently, IL-10 promotes mitophagy that eliminates dysfunctional mitochondria cha

270 nergetic stress providing protection against mitophagy that may preserve residual mitochondrial funct

271 Before the onset of mitophagy, the pathway blocks mitochondrial motility by

272 ociated mouse RGC differentiation depends on mitophagy, the programmed autophagic clearance of mitoch

273 Mitophagy, the selective engulfment of dysfunctional mit

274 Here, we report that mitophagy, the selective removal of mitochondria by auto

275 hondrial turnover is principally mediated by mitophagy, the trafficking of damaged mitochondria to ly

276 To initiate mitophagy, the ubiquitin kinase PINK1 phosphorylates ubi

277 itochondrial function in part by controlling mitophagy through Clec16a.

278 new mechanism of signal amplification during mitophagy through cooperative regulation of the TBK1 kin

279 Further, we explore how stimulating mitophagy through exercise may promote healthy ageing.

280 1 diabetes gene and itself a key mediator of mitophagy through regulation of the E3 ubiquitin ligase

281 itions effectively triggers Parkin-dependent mitophagy, thus establishing a foundation for further in

282 gations into cellular pathways in regulating mitophagy to ameliorate mitochondrial pathology in AD.

283 aperones, protein degradation, autophagy and mitophagy to maintain proteostasis and mitochondrial qua

284 d protein response and PINK1-Parkin-mediated mitophagy to mitigate proteotoxicity.

285 ore, it is important to assess autophagy and mitophagy together and separately.

286 The ability to assess mitophagy under a host of varying environmental and gene

287 NDC1, DRP1, or calnexin prevents fission and mitophagy under hypoxic conditions.

288 diating mitochondrial fission and subsequent mitophagy under hypoxic conditions.

289 cluding mitochondrial dynamics and autophagy/mitophagy, under high-glucose (HG) ambience or a diabeti

290 at healthy human neutrophils do not complete mitophagy upon induction of mitochondrial damage.

291 18-h time frame, as well as how to quantify mitophagy using the mt-Keima probe.

292 Furthermore, defective mitophagy was associated with an increased release of mi

293 Enhanced mitophagy was further confirmed in AD patient brains, ac

294 Mitochondrial autophagy (mitophagy) was also deficient in cells lacking TSC2, ass

295 ured neurons display Parkin-dependent axonal mitophagy, we find this is vanishingly rare in vivo unde

296 cause of the demand on lysosomal function by mitophagy, we investigated a role for the transcription

297 link between transcriptional repression and mitophagy, which is also apparent in human induced pluri

298 maged and dysfunctional mitochondria through mitophagy, which is dependent on the fission/fusion cycl

299 amics, mtDNA multiple deletions, and altered mitophagy with parkinsonism.

300 e USP8, and Clec16a, a mediator of beta-cell mitophagy with unclear function.