ReviewMolecular neurobiology2025
Potential Mechanisms of Exercise-Mediated Ferroptosis Regulation in Central Nervous System Diseases.
Review in Molecular neurobiology, 2025. 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
5 authors.
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Abstract
As a common health-promoting intervention, exercise is widely recommended for patients with central nervous system (CNS) disorders such as stroke, Parkinson's disease (PD), and Alzheimer's disease (AD). In current clinical practice, however, exercise intensity is often determined based on therapist experience, with low-to-moderate intensities typically chosen for safety reasons. Thus, clarifying the underlying mechanisms is essential for developing precise and personalized exercise prescriptions in the future. Evidence shows that exercise regulates various "exerkines" (e.g., BDNF, Nrf2, TNFAIP3, and SLC2A1), which promote neural repair and influence iron metabolism. Ferroptosis-an iron-dependent, programmed cell death distinct from apoptosis, necrosis, and autophagy-is closely associated with the progression and prognosis of many diseases, particularly those affecting the CNS. This review synthesizes current understanding of ferroptosis in stroke, PD, and AD, describes how key exercise parameters (intensity, type-aerobic vs. resistance, and duration) influence ferroptosis, and summarizes preclinical and clinical evidence on exercise-induced ferroptosis modulation in CNS disorders. Our aim is to provide a mechanistic basis for optimizing exercise prescriptions to enhance functional recovery in patients with CNS conditions.
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