ReviewFrontiers in cardiovascular medicine2026
Caveolin-1 in atherosclerosis: from endothelial lipoprotein transport to vascular immunometabolic remodeling.
Review in Frontiers in cardiovascular medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Atherosclerosis is initiated by endothelial dysfunction and pathological retention of apolipoprotein B-containing lipoproteins within the arterial intima, yet the molecular mechanisms governing the earliest steps of lipoprotein entry remain incompletely understood. Caveolin-1 (Cav-1), the principal structural component of endothelial caveolae, has emerged as a critical regulator of vascular lipid transport, mechanotransduction, and inflammatory remodeling. However, its diverse and sometimes opposing biological functions have prevented a unified understanding of its role in atherosclerosis. In this review, we integrate recent advances regarding Cav-1-mediated regulation of atherogenesis, focusing on the transition from endothelial lipoprotein transport to vascular immunometabolic remodeling. We first discuss the structural and biochemical properties of caveolae and the scaffolding functions of Cav-1 that organize signaling and transport platforms. We then examine how Cav-1-dependent caveolar transcytosis facilitates receptor-guided low-density lipoprotein (LDL) transport through scavenger receptor class B type 1 (SR-B1), activin receptor-like kinase 1 (ALK1), and the DOCK4-RAC1 trafficking pathway, thereby controlling early lipid deposition in the arterial wall. Furthermore, we summarize how disturbed flow, glycocalyx disruption, and impaired autophagic turnover regulate Cav-1 abundance and localization, linking vascular biomechanics to lipid handling capacity. Importantly, we highlight the cell type- and disease stage-dependent effects of Cav-1. While endothelial Cav-1 promotes atherogenesis by enabling LDL transcytosis, macrophage Cav-1 deficiency may enhance Toll-like receptor 4/nuclear factor-
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