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Life sciences · Journal article
Journal of the American Heart Association · October 23, 2026
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Anthracyclines are essential anticancer agents, yet a cardiomyocyte‐centered model incompletely explains why cardiac injury can be delayed, progressive, and poorly captured by resting ejection fraction. We frame anthracycline cardiotoxicity as a multicellular network failure within the cardiac niche: the spatially organized interactions among cardiomyocytes, fibroblasts, endothelial and immune cells, extracellular matrix, and circulating signals. Cardiomyocyte stress initiates injury, whereas pathological communication may propagate it. We distinguish a fibroblast–CD8 + T‐cell adhesion circuit, supported by loss‐of‐function evidence in mice and correlative human data, from an emerging therapy–conditioned tumor–heart extracellular vesicle axis supported mainly by breast cancer models. These pathways may converge on fibrotic stiffness, microvascular dysfunction, and electrical uncoupling; however, direct cross‐circuit interaction and drug‐independent sufficiency remain unproven. We integrate established clinical risk modifiers with this framework, specify causal criteria, and propose spatial multiomics, living myocardial slices, tumor‐bearing systems, and longitudinal phenotyping to test circuit persistence. This evidence‐calibrated model shifts the goal from cataloging cell‐intrinsic pathways to identifying mechanism‐resolved biomarkers and therapeutically targetable communication nodes while preserving antitumor efficacy.