HIF1α/MIF/CD74 signaling mediated OSA-induced atrial fibrillation by promoting M1 macrophages polarization

Increased polarization of M1-type macrophages was involved in the increased susceptibility to AF induced by OSA. In mechanism, OSA increased MIF expression by HIF1α in atrial myocytes. Then, MIF activated NF-κB expression by CD74 in macrophages, consequently driving the polarization of M1-type macrophages. Finally, M1 macrophages exacerbated atrial remodeling through the secretion of inflammatory cytokines, which contributed to the increased susceptibility to AF.