HIMF deletion ameliorates acute myocardial ischemic injury by promoting macrophage transformation to reparative subtype.

ABSTRACT: Appropriately manipulating macrophage M1/M2 phenotypic transition is a promising therapeutic strategy for tissue repair after myocardial infarction (MI). Here we showed that gene ablation of hypoxia-induced mitogenic factor (HIMF) in mice (Himf^-/- and HIMF^flox/flox;Lyz2-Cre) attenuated M1 macrophage-dominated inflammatory response and promoted M2 macrophage accumulation in infarcted hearts. This in turn reduced myocardial infarct size and improved cardiac function after MI. Correspondingly, expression of HIMF in macrophages induced expression of pro-inflammatory cytokines; the culturing medium of HIMF-overexpressing macrophages impaired the cardiac fibroblast viability and function. Furthermore, macrophage HIMF was found to up-regulate C/EBP-homologous protein (CHOP)

SUBMITTER: Li Y 

PROVIDER: S-EPMC8064941 | biostudies-literature | 2021 Apr

REPOSITORIES: biostudies-literature