ArticleRedox biology2024
Endurance exercise preconditioning alleviates ferroptosis induced by doxorubicin-induced cardiotoxicity through mitochondrial superoxide-dependent AMPKα2 activation.
Article in Redox biology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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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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Who cites it
19 citing papers in PubMed, 25 citations in OpenAlex.
- Aerobic Exercise Alleviates Oligodendrocyte Injury and Ferroptosis-Related Features in MPTP-Induced Parkinsonian Mice with Improved Neuropathological Phenotypes.Brain sciences · 2026Article
- Aerobic Exercise-Mediated Regulation of Ferroptosis in Skeletal Disorders: Molecular Mechanisms and Potential Applications.Biomolecules · 2026Review
- Exercise Preconditioning Activates AMPK-ACC Signaling and Attenuates Myocardial Ischemia/Reperfusion-Induced Ferroptosis.Journal of cardiovascular translational research · 2026Article
- Exploring the role of CaMKII in exercise-induced cardioprotection.Human cell · 2026Review
- Chemokine-Guided Biomimetic Mn/Ce Nanozymes for Immunomodulation and Cardioprotection in Doxorubicin-Induced Cardiomyopathy.Advanced healthcare materials · 2026Article
- Article
- Ferroptosis in Doxorubicin-Induced Cardiotoxicity: From Molecular Mechanisms to Therapeutic Strategies and Clinical Management Paradigms.Reviews in cardiovascular medicine · 2026Review
- VCPIP1 drives diabetic cardiomyopathy by deubiquitinating AMPKγ1 and preventing AMPKα-γ subunit assembly in cardiomyocytes.Signal transduction and targeted therapy · 2026Article
- Exercise modulates redox homeostasis in cardiovascular and metabolic diseases: from bench to clinic.Cardiovascular diabetology · 2026Review
- Does exercise modulate ferroptosis-related cardiovascular injury? Mechanistic evidence and translational boundaries.Frontiers in physiology · 2026Review
- Alteration of cardiac energetics and mitochondrial function in doxorubicin‑induced cardiotoxicity: Molecular mechanism and prospective implications (Review).International journal of molecular medicine · 2025Review
- The Role of ROS-Mediated Mitochondrial Dysfunction in the Development of Malignant Melanoma.Experimental dermatology · 2025Review
- The regulatory role of exercise in heart failure and myocardial energy metabolism: A review.Biomolecules & biomedicine · 2025Review
- Aerobic Exercise Activates Fibroblast Growth Factor 21 and Alleviates Cardiac Ischemia/Reperfusion-induced Neuronal Oxidative Stress and Ferroptosis in Paraventricular Nucleus.Molecular neurobiology · 2025Article
- Doxorubicin-Induced Cardiotoxicity: A Comprehensive Update.Journal of cardiovascular development and disease · 2025Review
- Integrating melt electrospinning writing and microfluidics to engineer a human cardiac microenvironment for high-fidelity drug screening.Bioactive materials · 2025Article
- Exercise in atherosclerosis: its beneficial effects and underlying mechanism.Frontiers in cell and developmental biology · 2025Review
- Isoform-specific roles of AMP-activated protein kinase in cardiac physiology and pathophysiology.Frontiers in cardiovascular medicine · 2025Review
- Ferroptosis in NAFLD: insights and the therapeutic potential of exercise.Frontiers in medicine · 2025Review
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Doxorubicin-induced cardiotoxicity (DIC) adversely impacts patients' long-term health and quality of life. Its underlying mechanism is complex, involving regulatory cell death mechanisms, such as ferroptosis and autophagy. Moreover, it is a challenge faced by patients undergoing cardiac rehabilitation. Endurance exercise (E-Exe) preconditioning effectively counters DIC injury, potentially through the adenosine monophosphate-activated protein kinase (AMPK) pathway. However, detailed studies on this process's mechanisms are scarce. Here, E-Exe preconditioning and DIC models were established using mice and primary cultured adult mouse cardiomyocytes (PAMCs). Akin to ferrostatin-1 (ferroptosis inhibitor), rapamycin (autophagic inducer), and MitoTEMPO (mitochondrial free-radical scavenger), E-Exe preconditioning effectively alleviated Fe
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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.