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DNA-damaging chemotherapy reshapes cardiac-resident macrophage composition and function
Journal article   Peer reviewed

DNA-damaging chemotherapy reshapes cardiac-resident macrophage composition and function

Ruijun He, Farid F Kadyrov, Andrew L Koenig, Pan Ma, Andrea Bredemeyer, Mandy M Chan, Joel D Schilling, Shibali Das, Joseph S Lagas, Daniel Kreisel, …
Science immunology, Vol.11(115), p.eadu4944
01/02/2026
DOI: 10.1126/sciimmunol.adu4944
PMID: 41481697

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Abstract

Heart failure and ischemic heart disease represent prevalent causes of death among cancer survivors. Despite extensive use of conventional chemotherapies, a limited understanding of how these agents affect the cardiac immune landscape exists. Using mouse models, we show that DNA-damaging agents selectively deplete cardiac-resident macrophages through activation of p53 signaling and resultant necroptosis and apoptosis. Genetic lineage tracing, transcriptomic profiling, and functional studies revealed that recruited monocytes progressively reconstitute the cardiac-resident macrophage compartment, were transcriptionally distinct from embryonic-derived cardiac-resident macrophages, and conferred protection from subsequent hypertensive and ischemic cardiac injury in mice. Monocyte-derived resident-like cardiac macrophages suppressed inflammation and attenuated adverse myocardial remodeling through a type I interferon-dependent mechanism. Collectively, these findings highlight unrecognized effects of DNA-damaging chemotherapies on the cardiac immune landscape and shed light on our understanding of monocyte plasticity and resident macrophage dynamics.
Animals Antineoplastic Agents - pharmacology DNA Damage - drug effects Macrophages - drug effects Macrophages - immunology Male Mice Mice, Inbred C57BL Monocytes - immunology Myocardium - immunology Myocardium - pathology Tumor Suppressor Protein p53 - metabolism

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