Macrofaag-PRMT9 verbetert uitkomsten na acuut myocardinfarct via STAT1-degradatie

BACKGROUND:During myocardial infarction (MI), M1-like macrophages exacerbate myocardial injury by excessively secreting inflammatory cytokines. Therefore, modulating the activity of M1-like macrophages may represent a novel therapeutic strategy for MI. PRMTs (protein arginine methyltransferases) primarily regulate protein function via asymmetric dimethylation, but PRMT9 does so through symmetric dimethylation. However, its role in cardiovascular diseases has yet to be established. In this study, we investigated the role of PRMT9 in macrophage polarization in the context of MI and explored its therapeutic effect for MI.METHODS:The correlation between PRMT9 in monocytes/macrophages and MI was investigated using the MI dataset GSE166780. Peripheral blood mononuclear cells were obtained from healthy individuals and patients with MI and analyzed to assess PRMT9 expression. We elucidated the functional role of PRMT9 in MI using macrophage-specificPrmt9knockout mice and macrophage-specific ov