Exercise Preconditioning Activates AMPK-ACC Signaling and Attenuates Myocardial Ischemia/Reperfusion-Induced Ferroptosis.
Y, X., J, T., C, W., R, L., Y, Z., M, C., & Z, T. (2026). Exercise Preconditioning Activates AMPK-ACC Signaling and Attenuates Myocardial Ischemia/Reperfusion-Induced Ferroptosis.. Journal of cardiovascular translational research. https://doi.org/10.1007/s12265-026-10828-x
Y X, J T, C W, R L, Y Z, M C, et al. Exercise Preconditioning Activates AMPK-ACC Signaling and Attenuates Myocardial Ischemia/Reperfusion-Induced Ferroptosis.. Journal of cardiovascular translational research. 2026; doi: 10.1007/s12265-026-10828-x
Y X, J T, C W, et al. Exercise Preconditioning Activates AMPK-ACC Signaling and Attenuates Myocardial Ischemia/Reperfusion-Induced Ferroptosis.[J]. Journal of cardiovascular translational research. 2026. DOI: 10.1007/s12265-026-10828-x.
@article{y2026,
author = {Xu Y and Tang J and Wu C and Li R and Zhao Y and Cai M and Tian Z},
title = {Exercise Preconditioning Activates AMPK-ACC Signaling and Attenuates Myocardial Ischemia/Reperfusion-Induced Ferroptosis.},
journal = {Journal of cardiovascular translational research},
year = {2026},
doi = {10.1007/s12265-026-10828-x},
note = {PMID: 42565937},
}
TY - JOUR AU - Xu Y AU - Tang J AU - Wu C AU - Li R AU - Zhao Y AU - Cai M AU - Tian Z TI - Exercise Preconditioning Activates AMPK-ACC Signaling and Attenuates Myocardial Ischemia/Reperfusion-Induced Ferroptosis. T2 - Journal of cardiovascular translational research PY - 2026 DO - 10.1007/s12265-026-10828-x AN - PMID:42565937 ER -
Ferroptosis critically mediates myocardial ischemia/reperfusion (I/R) injury. Exercise training confers cardioprotection, but whether it protects against I/R-induced ferroptosis and the underlying mechanisms remain unclear. In this study, C57BL/6J mice underwent six weeks of treadmill exercise preconditioning (EP) before myocardial I/R induction. Cardiac function, oxidative stress, ferroptosis markers and the phosphorylation of AMPK and ACC were assessed. In vitro, H9C2 cells were subjected to hypoxia/reoxygenation (H/R), and pharmacological modulators were used to investigate the necessity of the AMPK-ACC signaling. Results showed that EP alleviated I/R-induced cardiac dysfunction, reduced oxidative stress and iron deposition, upregulated GPX4 and SLC7A11 expression, downregulated ACSL4 expression, and enhanced the phosphorylation of AMPK and ACC. In H9C2 cells, H/R reduced ACC phosphorylation and induced ferroptosis. AMPK inhibition exacerbated H/R-induced ferroptosis, whereas AMPK activation by AICAR was protective. Critically, blocking ACC enzymatic activity attenuated AICAR's effects. These findings indicate that EP attenuates I/R-induced ferroptosis and the AMPK-ACC signaling may contribute to this protective effect.