Atherosclerosis (AS) is a chronic vascular disease characterized by lipid accumulation and the activation of the inflammatory response; it remains the leading nation-wide cause of death. Early in the progression of AS, stimulation by pro-inflammatory agonists (TNF-α, LPS, and others), oxidized lipoproteins (ox-LDL), and biomechanical stimuli (low shear stress) lead to endothelial cell activation and dysfunction. Consequently, it is crucial to investigate how endothelial cells respond to different stressors and ways to alter endothelial cell activation in AS development, as they are the earliest cells to respond. Caveolin-1 (Cav1) is a 21-24-kDa membrane protein located in caveolae and highly expressed in endothelial cells, which plays a vital role in regulating lipid transport, inflammatory responses, and various cellular signaling pathways and has atherogenic effects. This review summarizes recent studies on the structure and physiological functions of Cav1 and outlines the potential mechanisms it mediates in AS development. Included are the roles of Cav1 in the regulation of endothelial cell autophagy, response to shear stress, modulation of the eNOS/NO axis, and transduction of inflammatory signaling pathways. This review provides a rationale for proposing Cav1 as a novel target for the prevention of AS, as well as new ideas for therapeutic strategies for early AS.
Keywords: Atherosclerosis; Autophagy; Caveolin-1; Endothelial cells; Inflammation; eNOS/NO axis.
© 2023 The Authors.