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<p>The progression of myocardial ischemia-reperfusion injury (MIRI) is orchestrated by a decisive, bidirectional dialogue between mitochondrial reactive oxygen species (mtROS) and mitophagy. This review advances the concept of a dynamic “mtROS-mitophagy axis” as the central redox hub determining cardiomyocyte fate. We systematically dissect how moderate mtROS initiates protective mitophagy via key pathways (e.g., PINK1/Parkin, FUNDC1) and reinforces endogenous defenses through the Sirt3-FoxO3a integrator. Conversely, an mtROS burst disrupts this axis, triggering a vicious cycle of oxidative damage, impaired autophagic flux, and Drp1-mediated pathological fission. Critically, we emphasize the double-edged and temporally governed nature of this axis, arguing that its precise spatiotemporal modulation represents the next frontier in cardioprotection. Beyond mechanism, this synthesis provides a unified framework for developing novel therapies and for evaluating the cardiac safety of pharmacological agents, directly aligning with the core pursuits of cardiovascular redox biology and toxicology.</p> Graphical Abstract <p></p>

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The mtROS-Mitophagy Axis: A Decisive Redox Hub Governing Cell Fate in Myocardial Ischemia-Reperfusion Injury

  • 期刊论文

  • 发表日期：

    2026年7月11日

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  • Wei Wang,
  • Zhihao Xu,
  • Wei Liu,
  • Yaolu Kang,
  • Fan Zhang,
  • Qing Yu,
  • Ronglin Cai

摘要

The progression of myocardial ischemia-reperfusion injury (MIRI) is orchestrated by a decisive, bidirectional dialogue between mitochondrial reactive oxygen species (mtROS) and mitophagy. This review advances the concept of a dynamic “mtROS-mitophagy axis” as the central redox hub determining cardiomyocyte fate. We systematically dissect how moderate mtROS initiates protective mitophagy via key pathways (e.g., PINK1/Parkin, FUNDC1) and reinforces endogenous defenses through the Sirt3-FoxO3a integrator. Conversely, an mtROS burst disrupts this axis, triggering a vicious cycle of oxidative damage, impaired autophagic flux, and Drp1-mediated pathological fission. Critically, we emphasize the double-edged and temporally governed nature of this axis, arguing that its precise spatiotemporal modulation represents the next frontier in cardioprotection. Beyond mechanism, this synthesis provides a unified framework for developing novel therapies and for evaluating the cardiac safety of pharmacological agents, directly aligning with the core pursuits of cardiovascular redox biology and toxicology.

Graphical Abstract