Macrophage-derived KIF13B acts as a potential therapeutic target in atherosclerosis by enhancing MERTK-mediated efferocytosis [scRNA-Seq]

Atherosclerosis is a chronic inflammatory disorder with high morbidity and mortality rates worldwide. Emerging evidence has reported that Kinesin family member 13b (KIF13B), a crucial motor protein, integrates hepatic lipid metabolism and inflammatory response to protect liver disease. However, the relationship between KIF13B and atherosclerosis remains unknown. The present study aimed to elucidate the specific role of KIF13B in atherosclerosis and its potential therapeutic significance. Overall design: RNA-seq profiling of primary bone marrow-derived macrophages(BMDMs) extracted form WT(WT) and Kif13b-/-(KO) mice. For in vitro efferocytosis assessment, BMDMs were then co-cultured with apoptotic Jurkat cells(BMDMs with AC) at a 1:5 ratio (macrophages:apoptotic cells) for 90 minutes and also have WT(WA) and Kif13b-/- (KA)phenotype.