ReviewInternational journal of molecular sciences2026
Exercise-Mediated Regulation of Ferroptosis in Diabetic Cardiomyopathy: Mechanisms and Therapeutic Perspectives.
Review in International journal of molecular sciences, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
Abstract
Exercise is an important non-pharmacological intervention for the prevention and management of diabetes and its cardiovascular complications; however, the underlying mechanisms by which exercise confers cardiometabolic protection remain incompletely understood. Diabetic cardiomyopathy (DCM) is a major cardiovascular complication of diabetes, characterized by progressive myocardial structural and functional abnormalities associated with oxidative stress, dysregulated lipid metabolism, chronic inflammation, and miochondrial dysfunction. Ferroptosis, a form of regulated cell death characterized by iron-dependent lipid peroxidation, has emerged as a potential pathological link between metabolic disturbances and myocardial injury in DCM. Accumulating evidence suggests that exercise may modulate ferroptosis through multiple interconnected mechanisms, including restoration of iron homeostasis, suppression of lipid peroxidation, enhancement of endogenous antioxidant defenses, and improvement of mitochondrial function and quality control, thereby contributing to myocardial protection. In this review, we systematically summarize the cardioprotective benefits of exercise in the context of DCM and critically discuss the potential associations between exercise characteristics, including exercise modality, intensity, duration and the regulation of ferroptosis. By integrating current evidence on the molecular mechanisms underlying exercise-mediated ferroptosis regulation, this review provides a mechanistic framework for understanding how exercise may counteract ferroptosis in DCM and highlights the potential of ferroptosis-informed, precision exercise strategies for the prevention and management of diabetic cardiomyopathy.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.