Key result
Immune dysregulation via neutrophils, macrophages, and T cells drives doxorubicin-induced cardiotoxicity.
Why the study?
Clinical use of doxorubicin is limited by cardiotoxicity, and emerging evidence highlights a central role for immune dysregulation alongside direct myocardial injury in disease progression.
Highlights the central role of immune dysregulation in doxorubicin-induced cardiotoxicity, identifying potential immune targets for translational interventions to reduce cardiac injury.
Should not yet alter doxorubicin regimens; leaves open targeted immunomodulation trials.
Doxorubicin (DOX) remains a cornerstone in the treatment of various malignancies, but its clinical use is limited by cardiotoxicity, a leading cause of heart failure in cancer survivors. While oxidative stress and direct myocardial injury have long been implicated in DOX-induced cardiotoxicity (DIC), emerging evidence highlights the central role of immune dysregulation in disease progression. In particular, neutrophils, macrophages, and T cells orchestrate inflammatory responses that contribute to cardiomyocyte injury, adverse remodeling, and fibrosis. Recent findings also point to novel mediators that may serve as biomarkers or therapeutic targets. This review synthesizes current evidence on immune mechanisms underlying DIC and discusses how improved understanding of these pathways may inform immunomodulatory strategies to reduce cardiac injury without compromising anticancer efficacy.
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fraeyenhove et al. (2025) conducted a review in Doxorubicin-induced cardiotoxicity. Immune dysregulation involving neutrophils, macrophages, and T cells plays a central role in doxorubicin-induced cardiotoxicity, offering potential targets for immunomodulatory interventions.
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