ATF3 coordinates the survival and proliferation of cardiac macrophages and protects against ischemia-reperfusion injury.

ABSTRACT: Cardiac resident MerTK⁺ macrophages exert multiple protective roles after ischemic injury; however, the mechanisms regulating their fate are not fully understood. In the present study, we show that the GAS6-inducible transcription factor, activating transcription factor 3 (ATF3), prevents apoptosis of MerTK⁺ macrophages after ischemia-reperfusion (IR) injury by repressing the transcription of multiple genes involved in type I interferon expression (Ifih1 and Ifnb1) and apoptosis (Apaf1). Mice lacking ATF3 in cardiac macrophages or myeloid cells showed excessive loss of MerTK⁺ cardiac macrophages, poor angiogenesis and worse heart dysfunction after IR, which were rescued by the transfer of MerTK⁺ cardiac macrophages. GAS6 administration improved c

SUBMITTER: Shao Y 

PROVIDER: S-EPMC11358155 | biostudies-literature | 2024 Jan

REPOSITORIES: biostudies-literature