ReviewFrontiers in pharmacology2026
Ferroptosis regulation in doxorubicin-induced cardiotoxicity: multi-mechanism interventions and translational strategies.
Review in Frontiers in pharmacology, 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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6 authors.
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Abstract
Doxorubicin (DOX), a highly effective anthracycline chemotherapy drug, has its clinical application severely restricted by dose-dependent doxorubicin-induced cardiotoxicity (DIC). Ferroptosis, an iron-dependent, lipid peroxidation-driven regulated cell death, has been confirmed as a core pathological mechanism in DIC, where it synergistically participates with multiple cell death modalities in myocardial injury. This review systematically elaborates the multidimensional molecular mechanisms underlying DOX-induced myocardial ferroptosis, including: lipid peroxidation cascade self-amplification, bidirectional regulation by selective autophagy, multilayered GPX4 modification and stability regulation, and involvement of the gut microbiota-heart axis. Concurrently, we summarize evidence for natural phytochemicals-including flavonoids, polyphenols, terpenoids, and traditional Chinese medicine compounds-that inhibit myocardial ferroptosis via multi-target mechanisms, providing theoretical support for phytochemical-based DIC intervention. Critically, this review addresses the clinical translation dilemmas in ferroptosis regulation and proposes three innovative strategies: (1) time-decoupling strategy based on IFN-γ signaling; (2) cardiac-targeted nanodrug delivery system employing the OGF/OGFR axis; (3) cross-regulation between ferroptosis and other regulated cell death pathways. These strategies aim to achieve tissue-selective ferroptosis intervention, simultaneously protecting myocardium while maintaining DOX anti-tumor efficacy, thereby providing molecular mechanistic basis and clinical translational directions for constructing precision ferroptosis-targeted cardioprotective strategies.
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