Caveolin-1-mediated LDL transcytosis across endothelial cells in atherosclerosis

Atherosclerosis is widely recognized as a chronic inflammatory disease of the arterial wall characterized by the progressive accumulation of lipids, inflammatory cells, and fibrous material in the subendothelial space of large arteries. The occurrence and pathogenesis of atherosclerosis are intricately linked to the deposition of low-density lipoprotein (LDL) in the arterial wall. LDL must cross the intact endothelium to reach the subendothelial space, with caveolin-1 assuming a crucial role in this process. Caveolin-1 is a 21-24 kDa membrane protein located in caveolae and highly expressed in endothelial cells. Previous investigations have demonstrated the pivotal role of caveolin-1 in fostering atherosclerosis through its modulation of membrane trafficking, cholesterol metabolism, and cellular signaling. However, how caveolin-1 regulates LDL transcytosis across endothelial cells in atherosclerosis remains unclear. We provide a comprehensive overview of recent research on the interplay between caveolin-1 and atherosclerosis, with a specific focus on elucidating the role of caveolin-1 in mediating LDL transcytosis across endothelial cells. This review furnishes theoretical foundations supporting the pivotal role of caveolin-1 in both the inception and progression of atherosclerosis. It underscores the prospective viability of caveolin-1 as a new therapeutic target for atherosclerosis and introduces novel perspectives for treatment strategies in the early stages of atherosclerosis.