Self-renewing resident cardiac macrophages limit adverse remodeling following myocardial infarction.

ABSTRACT: Macrophages promote both injury and repair after myocardial infarction, but discriminating functions within mixed populations remains challenging. Here we used fate mapping, parabiosis and single-cell transcriptomics to demonstrate that at steady state, TIMD4⁺LYVE1⁺MHC-II^loCCR2^- resident cardiac macrophages self-renew with negligible blood monocyte input. Monocytes partially replaced resident TIMD4^-LYVE1^-MHC-II^hiCCR2^- macrophages and fully replaced TIMD4^-LYVE1^-MHC-II^hiCCR2⁺ macrophages, revealing a hierarchy of monocyte contribution to functionally distinct macrophage subsets. Ischemic injury reduced TIMD4⁺ and TIMD4^- resident macrophage

SUBMITTER: Dick SA 

PROVIDER: S-EPMC6565365 | biostudies-literature | 2019 Jan

REPOSITORIES: biostudies-literature