Key result
Exercise-induced cardiac rehab drives cardioprotection by modulating inflammation, oxidative stress, and mitochondrial biogenesis.
Why the study?
Cardiac rehabilitation benefits are primarily described by functional outcomes, leaving the underlying molecular basis less clearly integrated.
This review provides a conceptual framework for the molecular mechanisms underlying exercise-induced cardioprotection, supporting a biology-guided approach to individualized exercise prescription in cardiac rehabilitation.
Supports molecular exploration of exercise in cardiac recovery; leaves open translation to clinical outcomes.
Cardiac rehabilitation (CR), centered on structured exercise training, improves exercise capacity, cardiac function, and quality of life in patients with cardiovascular disease (CVD). However, its benefits are still described mainly by functional outcomes, whereas the underlying molecular basis remains less clearly integrated. This review summarizes the major mechanisms of exercise-induced cardioprotection in CR, including modulation of inflammation and oxidative stress, enhancement of mitochondrial biogenesis and quality control, improvement of endothelial function, regulation of epigenetic pathways, and release of exercise-derived factors. These interconnected responses influence cardiac remodeling, metabolic homeostasis, endothelial repair, and cell survival. We further integrate these mechanisms into a conceptual framework and discuss how different exercise stimuli may preferentially engage distinct biological pathways, supporting a mechanism-informed approach to individualized exercise prescription. A better understanding of these molecular networks may help advance CR from functional rehabilitation toward a more precise and biology-guided strategy.
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Ren et al. (2026) conducted a review in Cardiovascular disease (CVD). Exercise-induced cardiac rehabilitation was evaluated. Exercise-induced cardiac rehabilitation promotes cardioprotection through molecular mechanisms including modulation of inflammation, oxidative stress, and enhancement of mitochondrial biogenesis.
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