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Journal ArticleDOI

Mitophagy and mitochondrial integrity in cardiac ischemia-reperfusion injury.

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TLDR
This review will revisit the contemporary understanding of mitophagy in the regulation of cardiac homeostasis and update recent progresses with regards toMitophagy and cardiac IR injury to establish a role for Mitophagy as a potential therapeutic target in the management of IR injury.
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This article is published in Biochimica et Biophysica Acta.The article was published on 2019-09-01. It has received 128 citations till now. The article focuses on the topics: Mitophagy & Reperfusion injury.

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Citations
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Journal ArticleDOI

New insights into the role of mitochondria in cardiac microvascular ischemia/reperfusion injury.

TL;DR: The involvement of mROS and mitochondrial morphofunction in cardiac microvascular I/R injury is discussed.
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Mitochondrial quality control mechanisms as molecular targets in cardiac ischemia-reperfusion injury.

TL;DR: The regulatory mechanisms and pathological effects of MQC in myocardial I/R injury are summarized, highlighting potential targets for the clinical management of reperfusion.
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The Role of Mitochondria in the Mechanisms of Cardiac Ischemia-Reperfusion Injury

TL;DR: Various cardioprotective interventions that modulate mitochondrial stability, dynamics and turnover, including various pharmacologic agents, specific mitochondrial antioxidants and uncouplers, and ischemic preconditioning can be considered as the main strategies to protect mitochondrial and cardiovascular function and thus enhance longevity.
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Phosphoglycerate mutase 5 exacerbates cardiac ischemia-reperfusion injury through disrupting mitochondrial quality control.

TL;DR: In conclusion, the results provide an insight into the specific role and working mechanism of PGAM5 in driving cardiomyocyte necroptosis through imposing mitochondrial quality control in cardiac I/R injury.
References
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Journal ArticleDOI

p62/SQSTM1 Binds Directly to Atg8/LC3 to Facilitate Degradation of Ubiquitinated Protein Aggregates by Autophagy

TL;DR: It is demonstrated that the previously reported aggresome-like induced structures containing ubiquitinated proteins in cytosolic bodies are dependent on p62 for their formation and p62 is required both for the formation and the degradation of polyubiquitin-containing bodies by autophagy.

p62/SQSTM1 Binds Directly to Atg8/LC3 to Facilitate Degradation of Ubiquitinated Protein Aggregates

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.
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PINK1/Parkin-mediated mitophagy is dependent on VDAC1 and p62/SQSTM1

TL;DR: Functional links between PINK1, Parkin and the selective autophagy of mitochondria, which is implicated in the pathogenesis of Parkinson's disease, are provided.
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Ischemia and reperfusion—from mechanism to translation

TL;DR: Ischemia and reperfusion-elicited tissue injury contributes to morbidity and mortality in a wide range of pathologies, including myocardial infarction, ischemic stroke, acute kidney injury, trauma, circulatory arrest, sickle cell disease and sleep apnea as discussed by the authors.
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Physiological roles of mitochondrial reactive oxygen species.

TL;DR: More and more evidence suggests that mROS are critical for healthy cell function, and this evidence is discussed following some background on the generation and regulation ofmROS.
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