Mmu_circ_0001148 promotes endothlial-mesenchymal transition via regulating miR-218-5p/JMY axis and drives progression of atherosclerosis.

Atherosclerosis (AS) is a common cardiovascular disease and responsible for the high mortality of cardiovascular emergencies. Circular RNAs (circRNAs) show a potential role in atherogenesis. We identified an aberrantly expressed circRNA (circ_0001148) in atherosclerotic tissues. However, whether circ_0001148 involved in atherogenesis remains unclear. The present study aimed to investigate the biological function of circ_0001148 and the underlying mechanism in AS. Functional analysis indicated that circ_0001148 promoted endothelial-mesenchymal transition (EndMT) and thus accelerated the formation of atherosclerotic plaque. The mechanism analysis suggested that circ_0001148 act as a competitive endogenous RNA (ceRNA) to modify the expression of JMY by sponging miR-218-5p. We also demonstrated that the treatment of miR-218-5p mimics or JMY deficiency could attenuated the progression of AS induced by circ_0001148 overexpression. Therefore, we proposed a novel signaling network which circ_0001148 promotes atherogenesis via miR-218-5p/JMY axis. These findings provide new insights into the mechanisms of AS, and potentially leading to the development of a novel therapeutic strategy targeting circ_0001148.