Aerobic exercise enhances mitochondrial resilience and iron homeostasis, offering non-pharmacological protection against ferroptosis in aging cardiomyocytes.
Does aerobic exercise prevent ferroptosis in aging cardiomyocytes?
Aerobic exercise offers a promising non-pharmacological strategy to mitigate age-related cardiac dysfunction by suppressing ferroptosis via the Parkin-ACSL4 axis and improving iron homeostasis.
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Abstract Ferroptosis, iron-dependent regulated cell death, drives age-related cardiac dysfunction. This review examines aerobic exercise modulation of ferroptosis in aging cardiomyocytes via Parkin–ACSL4 axis. Parkin promotes ACSL4 ubiquitination/degradation, reducing lipid peroxidation and ROS. Exercise activates PINK1/Parkin mitophagy and hepcidin, enhancing mitochondrial resilience and iron homeostasis. Despite promising preclinical evidence, molecular mechanisms remain unclear. Aerobic exercise offers non-pharmacological cardiac protection against ferroptosis in aging.
Kordi et al. (Tue,) reported a other. Aerobic exercise enhances mitochondrial resilience and iron homeostasis, offering non-pharmacological protection against ferroptosis in aging cardiomyocytes.