Abstract

The mammalian target of rapamycin (mTOR) regulates multiple pathophysiological processes, such as cell development, angiogenesis, autophagy, as well as innate-adaptive immune responses. Numerous studies have demonstrated that mTOR signaling plays an important role in the process of atherosclerosis (AS) itself or AS-related diseases. The activation of mTOR signaling contributes to the endothelium dysfunction and the formation of foam cells via enhancing the process from monocyte to macrophage in the initial stage of atherosclerosis. The activation of mTOR signaling not only promotes the formation of the fatty streak (more foam cells), and migration and proliferation of vascular smooth muscle cells in the early lesion of AS, but also facilitates the formation of vulnerable plaque and replication of vascular smooth muscle cells in the late lesion of AS. Moreover, it has been found the role of the upstream and downstream components of mTOR signaling pathway in the formation of AS. Thus, the mTOR inhibitors may be a promising target for the prevention and treatment of AS.

Keywords: Mammalian target of rapamycin, atherosclerosis, mTOR signaling, foam cell, macrophage, vascular smooth muscle cells.