ReviewFrontiers in physiology2026
Does exercise modulate ferroptosis-related cardiovascular injury? Mechanistic evidence and translational boundaries.
Review in Frontiers in physiology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Authors and funding
8 authors.
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Abstract
Ferroptosis connects disrupted iron handling, phospholipid peroxidation, and insufficient antioxidant defense with cardiovascular injury. Whether exercise can modify ferroptosis-related vulnerability in the heart and vasculature remains an important but incompletely resolved question. This mechanism-centered narrative review evaluates exercise-related evidence across cardiovascular injury contexts and distinguishes direct cardiovascular experiments from supportive marker studies, indirect mechanistic evidence, and human clinical contexts. PubMed was searched through June 2026, with supplementary retrieval from the Web of Science Core Collection and citation tracing. Among available exercise-specific studies, current evidence is most informative in preclinical models, particularly doxorubicin cardiotoxicity, where endurance exercise preconditioning has been linked to reduced iron accumulation, lipid-peroxide injury, mitochondrial damage, and myocardial dysfunction in studies incorporating ferroptosis-sensitive perturbation. Additional evidence from ischemia-reperfusion injury, diabetic cardiomyopathy, cardiac fibrosis, and experimental heart failure suggests that exercise may influence iron handling, the system Xc
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