Mitochondrial quality surveillance as a therapeutic target in myocardial infarction

Hang Zhu, Sam Toan, David Mui, Hao Zhou

Research output: Contribution to journalReview articlepeer-review

99 Scopus citations


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.

Original languageEnglish (US)
Article numbere13590
JournalActa Physiologica
Issue number3
StatePublished - Dec 16 2020

Bibliographical note

Funding Information:
This study was supported by grants from the National Natural Science Foundation of China (No. 81900252, 81870249 and 82000537). The funders had no role in the study design, data collection and analysis, decision to publish or preparation of the manuscript.

Publisher Copyright:
© 2020 Scandinavian Physiological Society. Published by John Wiley & Sons Ltd


  • fission
  • fusion
  • mitochondria-dependent cell death
  • mitochondrial quality surveillance
  • mitophagy
  • myocardial infarction

PubMed: MeSH publication types

  • Journal Article
  • Research Support, Non-U.S. Gov't
  • Review


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