Journal ArticleDOI
Mitochondrial quality surveillance as a therapeutic target in myocardial infarction.
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TLDR
The recent findings focusing on the role of mitochondrial quality Surveillance in MI are discussed, and the available therapeutic approaches targeting mitochondrial quality surveillance during MI are highlighted.Abstract:
Myocardial infarction (MI) is a leading cause of morbidity and mortality worldwide. As mitochondrial dysfunction critically contributes to the pathogenesis of MI, intensive research is focused on the development of therapeutic strategies targeting mitochondrial homeostasis. Mitochondria possess a quality control system which maintains and restores their structure and function by regulating mitochondrial fission, fusion, biogenesis, degradation and death. In response to slight damage such as transient hypoxia or mild oxidative stress, mitochondrial metabolism shifts from oxidative phosphorylation to glycolysis, in order to reduce oxygen consumption and maintain ATP output. Mitochondrial dynamics are also activated to modify mitochondrial shape and structure, in order to meet cardiomyocyte energy requirements through augmenting or reducing mitochondrial mass. When damaged mitochondria cannot be repaired, poorly structured mitochondria will be degraded through mitophagy, a process which is often accompanied by mitochondrial biogenesis. Once the insult is severe enough to induce lethal damage in the mitochondria and the cell, mitochondrial death pathway activation is an inevitable consequence, and the cardiomyocyte apoptosis or necrosis program will be initiated to remove damaged cells. Mitochondrial quality surveillance is a hierarchical system preserving mitochondrial function and defending cardiomyocytes against stress. A failure of this system has been regarded as one of the potential pathologies underlying MI. In this review, we discuss the recent findings focusing on the role of mitochondrial quality surveillance in MI, and highlight the available therapeutic approaches targeting mitochondrial quality surveillance during MI.read more
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Mitophagy coordinates the mitochondrial unfolded protein response to attenuate inflammation-mediated myocardial injury.
TL;DR: In this paper, the authors showed that mitophagy and the mitochondrial unfolded protein response (UPRmt) are the predominant stress-responsive and protective mechanisms involved in repairing damaged mitochondria in sepsis-induced myocardial injury.
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Irisin Attenuates Oxidative Stress, Mitochondrial Dysfunction, and Apoptosis in the H9C2 Cellular Model of Septic Cardiomyopathy through Augmenting Fundc1-Dependent Mitophagy.
TL;DR: In this article, irisin treatment attenuates septic cardiomyopathy via Fundc1-related mitophagy, and irisin significantly increased ATP production and the activities of mitochondrial complexes I and III.
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Empagliflozin attenuates cardiac microvascular ischemia/reperfusion through activating the AMPKα1/ULK1/FUNDC1/mitophagy pathway
C Cai,Zhongzhou Guo,Xing Chang,Ziying Li,Feng Wu,Jing He,Tiantian Cao,Kangrong Wang,Nengxian Shi,Hao Zhou,Sam Toan,David Muid,Yi-Peng Tan +12 more
TL;DR: In this paper , empagliflozin could reduce cardiac microvascular ischemia/reperfusion (I/R) injury by enhancing mitophagy in mice.
Journal ArticleDOI
SIRT5-Related Desuccinylation Modification Contributes to Quercetin-Induced Protection against Heart Failure and High-Glucose-Prompted Cardiomyocytes Injured through Regulation of Mitochondrial Quality Surveillance.
Xing Chang,Tian Zhang,Junyan Wang,Yan Liu,Peizheng Yan,Qingyan Meng,Yongtian Yin,Shiyuan Wang +7 more
TL;DR: In this article, the authors investigated whether SIRT5 and IDH2-related desuccinylation is involved in the underlying mechanism of myocardial fibrosis in heart failure while exploring related therapeutic drugs for mitochondrial quality surveillance.
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TL;DR: New insights into interactions among BCL-2 family proteins reveal how these proteins are regulated, but a unifying hypothesis for the mechanisms they use to activate caspases remains elusive.
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p62/SQSTM1 Binds Directly to Atg8/LC3 to Facilitate Degradation of Ubiquitinated Protein Aggregates by Autophagy
Serhiy Pankiv,Terje Høyvarde Clausen,Trond Lamark,Andreas Brech,Jack-Ansgar Bruun,Heidi Outzen,Aud Øvervatn,Geir Bjørkøy,Terje Johansen +8 more
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Journal ArticleDOI
Molecular mechanisms of cell death: recommendations of the Nomenclature Committee on Cell Death 2018.
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TL;DR: The Nomenclature Committee on Cell Death (NCCD) has formulated guidelines for the definition and interpretation of cell death from morphological, biochemical, and functional perspectives.
p62/SQSTM1 Binds Directly to Atg8/LC3 to Facilitate Degradation of Ubiquitinated Protein Aggregates
Serhiy Pankiv,Terje Høyvarde Clausen,Trond Lamark,Andreas Brech,Jack-Ansgar Bruun,Heidi Outzen,Aud Øvervatn,Geir Bjørkøy,Terje Johansen,Fromthe ‡ BiochemistryDepartment +9 more
TL;DR: In this article, the authors showed that the polyubiquitin-binding protein p62/SQSTM1 is degraded by autophagy by using a 22-residue sequence of p62 containing an evolutionarily conserved motif.