Abstract
Aortic stiffness during cardiac contraction is defined by the rigidity of the aorta and the elastic resistance to deformation. Recent studies suggest that aortic stiffness may be associated with changes in cholesterol efflux in endothelial cells. This alteration in cholesterol efflux may directly affect endothelial function, extracellular matrix composition, and vascular smooth muscle cell function and behavior. These pathological changes favor an aortic stiffness phenotype. Among all of the proteins participating in the cholesterol efflux process, ATP binding cassette transporter A1 (ABCA1) appears to be the main contributor to arterial stiffness changes in terms of structural and cellular function. ABCA1 is also associated with vascular inflammation mediators implicated in aortic stiffness. The goal of this mini review is to provide a conceptual hypothesis of the recent advancements in the understanding of ABCA1 in cholesterol efflux and its role and association in the development of aortic stiffness, with a particular emphasis on the potential mechanisms and pathways involved.
Highlights
Arterial stiffness develops from a complex interaction between stable and dynamic changes involving structural and cellular elements of the vessel wall
ATP binding cassette transporter A1 (ABCA1) gene mutation carriers are characterized by increased intima-media thickness [74,75], while ABCA1-dependent cholesterol efflux is inversely correlated with pulse wave velocity (PWV) in healthy subjects [76]
A marked variability in Apo A1 binding and Apo A1-mediated cholesterol efflux has been observed across different vascular smooth muscle cells (VSMCs) phenotypes, which exhibit different levels of contractility and rates of synthesis of extracellular matrix (ECM) components including collagens, elastin, proteoglycans, cadherins, and integrins that regulate the stiffness of vessels [5,80,81]
Summary
Arterial stiffness develops from a complex interaction between stable and dynamic changes involving structural and cellular elements of the vessel wall. Aortic stiffness is a consequence of pathophysiological alterations involving endothelial cells, vascular smooth muscle cells (VSMCs), extracellular matrix (ECM), inflammatory responses, and other functional elements [1]. A stiffened aorta, as a consequence of fractures of the elastic lamina, replacement of elastin by collagens, local inflammation, VSMC infiltration, necrosis, and calcification, opposes systolic distention. When this occurs, hemodynamic factors require a greater amount of force to accommodate the stroke volume, which leads to an increase in systolic blood pressure and a decrease in diastolic blood pressure, and high pulse pressure. Cholesterol efflux affects endothelial cells, ECM composition, and VSMC function and behavior [20,21], suggesting an intimacy between arterial stiffness and the cholesterol efflux in cardiovascular diseases
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