BNIP3L/NIX-mediated mitophagy protects against ischemic brain injury independent of PARK2.
Yang Yuan,Yanrong Zheng,Xiangnan Zhang,Ying Chen,Xiaoli Wu,Jiaying Wu,Zhe Shen,Lei Jiang,Lu Wang,Wei Yang,Jianhong Luo,Zheng-Hong Qin,Weiwei Hu,Zhong Chen +13 more
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TLDR
The involvement of BNIP3L/NIX in cerebral ischemia-reperfusion (I-R)-induced mitophagy is identified and insights into mitochondrial quality control in ischemic stroke are offered.Abstract:
Cerebral ischemia induces massive mitochondrial damage. These damaged mitochondria are cleared, thus attenuating brain injury, by mitophagy. Here, we identified the involvement of BNIP3L/NIX in cer...read more
Citations
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Journal ArticleDOI
Molecular mechanisms and physiological functions of mitophagy.
TL;DR: In this article, the authors review the current molecular understanding of mitophagy, and its physiological implications, and discuss how multiple mitophathy pathways coordinately modulate mitochondrial fitness and populations.
Journal ArticleDOI
A Molecular Approach to Mitophagy and Mitochondrial Dynamics.
Seung-Min Yoo,Yong-Keun Jung +1 more
TL;DR: The roles of mitophagy adapters and receptors in the recognition of damaged mitochondria by autophagosomes are focused on and a functional association ofmitophagy with mitochondrial dynamics through the interaction ofMitophagy adaptor and receptor proteins with mitochondrial fusion and fission proteins is addressed.
Journal ArticleDOI
PINK1-parkin pathway of mitophagy protects against contrast-induced acute kidney injury via decreasing mitochondrial ROS and NLRP3 inflammasome activation.
Qisheng Lin,Shu Li,Na Jiang,Xinghua Shao,Minfang Zhang,Haijiao Jin,Zhen Zhang,Jianxiao Shen,Yijun Zhou,Wenyan Zhou,Leyi Gu,Renhua Lu,Zhaohui Ni +12 more
TL;DR: It is demonstrated that PINK1-Parkin–mediated mitophagy played a protective role in CI-AKI by reducing NLRP3 inflammasome activation and preventing RTEC apoptosis, tissue damage, mitochondrial damage, and renal injury under contrast exposure were more severe in Pink1- or PARK2-deficient cells and mice than in wild-type groups.
Journal ArticleDOI
Autophagy in ischemic stroke.
TL;DR: A crosstalk between autophagy, necroptosis, and apoptosis that contribute to ischemic stroke is proposed and the interactions between Autophagy and oxidative stress, mitochondrial dysfunction and endoplasmic reticulum stress are discussed.
Journal ArticleDOI
Protective role of melatonin in cardiac ischemia-reperfusion injury: From pathogenesis to targeted therapy
TL;DR: The research progress related to IR injury is summarized, the possible mechanisms responsible for the myocardial benefits of melatonin against reperfusion injury are listed and the prospect of the use ofmelatonin in clinical application is discussed.
References
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Journal ArticleDOI
Parkin is recruited selectively to impaired mitochondria and promotes their autophagy
TL;DR: It is shown that Parkin is selectively recruited to dysfunctional mitochondria with low membrane potential in mammalian cells and this recruitment promotes autophagy of damaged mitochondria and implicate a failure to eliminate dysfunctional mitochondira in the pathogenesis of Parkinson's disease.
Journal ArticleDOI
The ubiquitin kinase PINK1 recruits autophagy receptors to induce mitophagy
Michael Lazarou,Danielle A. Sliter,Lesley A. Kane,Shireen A. Sarraf,Chunxin Wang,Jonathon L. Burman,Dionisia P. Sideris,Adam I. Fogel,Richard J. Youle +8 more
TL;DR: Using genome editing to knockout five autophagy receptors in HeLa cells, this work shows that two receptors previously linked to xenophagy, NDP52 and optineurin, are the primary receptors for PINK1- and parkin-mediated mitophagy.
Journal ArticleDOI
Ischaemic accumulation of succinate controls reperfusion injury through mitochondrial ROS.
Edward T. Chouchani,Edward T. Chouchani,Victoria R. Pell,Edoardo Gaude,Dunja Aksentijevic,Stephanie Y. Sundier,Ellen L. Robb,Angela Logan,Sergiy M. Nadtochiy,Emily N.J. Ord,Anthony C. Smith,Filmon Eyassu,Rachel Shirley,Chou Hui Hu,Anna J. Dare,Andrew M. James,Sebastian Rogatti,Richard C. Hartley,Simon Eaton,Ana S. H. Costa,Paul S. Brookes,Sean M. Davidson,Michael R. Duchen,Kourosh Saeb-Parsy,Michael J. Shattock,Alan J. Robinson,Lorraine M. Work,Christian Frezza,Thomas Krieg,Michael P. Murphy +29 more
TL;DR: In this article, a comparative in vivo metabolomic analysis was conducted to identify widely conserved metabolic pathways responsible for mitochondrial reactive oxygen species (ROS) production during ischaemia reperfusion.
Journal ArticleDOI
Mitochondrial outer-membrane protein FUNDC1 mediates hypoxia-induced mitophagy in mammalian cells
Lei Liu,Du Feng,Guo Chen,Ming Chen,Qiaoxia Zheng,Pingping Song,Qi Ma,Chongzhuo Zhu,Rui Wang,Wanjun Qi,Lei Huang,Peng Xue,Baowei Li,Xiaohui Wang,Haijing Jin,Jun Wang,Fuquan Yang,Pingsheng Liu,Yushan Zhu,Sen-Fang Sui,Quan Chen,Quan Chen +21 more
TL;DR: It is reported that FUNDC1, an integral mitochondrial outer-membrane protein, is a receptor for hypoxia-induced mitophagy, and its findings offer insights into mitochondrial quality control in mammalian cells.
Ischaemic accumulation of succinate controls reperfusion injury through mitochondrial ROS
EE Chouchani,Pell,Edoardo Gaude,Dunja Aksentijevic,Stephanie Y. Sundier,Michael R. Duchen,Michael J. Shattock,Christian Frezza,Thomas Krieg,Michael P. Murphy +9 more
TL;DR: It is shown that selective accumulation of the citric acid cycle intermediate succinate is a universal metabolic signature of ischaemia in a range of tissues and is responsible for mitochondrial ROS production during reperfusion, and a new pathway for metabolic control of ROS production in vivo is revealed.