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Resolving the links between efferocytosis and DNMT3A mutation-driven clonal hematopoiesis in atherosclerosis.

Created on 16 Oct 2026

Authors

Aarti Asnani

Published in

The Journal of clinical investigation. Volume 136. Issue 20. Oct 15, 2026. Epub Oct 15, 2026.

Abstract

Efferocytosis, or the clearance of apoptotic cells by macrophages, has been implicated in tissue resolution that promotes disease regression in atherosclerosis and other diseases of chronic inflammation. The mechanisms by which efferocytosis leads to pro-resolving macrophage reprogramming have not been fully defined. In this issue of the JCI, Avrampou and colleagues found that efferocytosis activates DNA-methyltransferase-3A (DNMT3A) to promote base excision repair and suppress oxidized DNA. Moreover, they provide evidence that DNMT3A enabled tissue repair in the context of plaque regression in a mouse model of atherosclerosis. Human studies have linked DNMT3A mutation-mediated clonal hematopoiesis (DNMT3A-CH) with atherosclerosis. The findings of Avrampou et al. linking DNMT3A function to efferocytosis-mediated tissue repair suggest that this pathway could be modulated therapeutically to minimize cardiovascular events in patients.

PMID:
42878086
Bibliographic data and abstract were imported from PubMed on 16 Oct 2026.

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