The mtROS-Mitophagy Axis: A Decisive Redox Hub Governing Cell Fate in Myocardial Ischemia-Reperfusion Injury.
W, W., Z, X., W, L., Y, K., F, Z., Q, Y., & R, C. (2026). The mtROS-Mitophagy Axis: A Decisive Redox Hub Governing Cell Fate in Myocardial Ischemia-Reperfusion Injury.. Cardiovascular toxicology. https://doi.org/10.1007/s12012-026-10137-4
W W, Z X, W L, Y K, F Z, Q Y, et al. The mtROS-Mitophagy Axis: A Decisive Redox Hub Governing Cell Fate in Myocardial Ischemia-Reperfusion Injury.. Cardiovascular toxicology. 2026; doi: 10.1007/s12012-026-10137-4
W W, Z X, W L, et al. The mtROS-Mitophagy Axis: A Decisive Redox Hub Governing Cell Fate in Myocardial Ischemia-Reperfusion Injury.[J]. Cardiovascular toxicology. 2026. DOI: 10.1007/s12012-026-10137-4.
@article{w2026,
author = {Wang W and Xu Z and Liu W and Kang Y and Zhang F and Yu Q and Cai R},
title = {The mtROS-Mitophagy Axis: A Decisive Redox Hub Governing Cell Fate in Myocardial Ischemia-Reperfusion Injury.},
journal = {Cardiovascular toxicology},
year = {2026},
doi = {10.1007/s12012-026-10137-4},
note = {PMID: 42435142},
}
TY - JOUR AU - Wang W AU - Xu Z AU - Liu W AU - Kang Y AU - Zhang F AU - Yu Q AU - Cai R TI - The mtROS-Mitophagy Axis: A Decisive Redox Hub Governing Cell Fate in Myocardial Ischemia-Reperfusion Injury. T2 - Cardiovascular toxicology PY - 2026 DO - 10.1007/s12012-026-10137-4 AN - PMID:42435142 ER -
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.