Abstract
Atherosclerosis and its complications diseases remain leading causes of cardiovascular morbidity and mortality, bringing a massive burden on public health worldwide. Atherosclerosis is recognized as chronic inflammation, and involves several highly correlated processes, including lipid metabolism dysfunction, endothelial cell dysfunction, inflammation, oxidative stress, vascular smooth muscle cell activation, platelet activation, thrombosis, altered matrix metabolism, and vascular remodeling. Within the past few decades, accumulating evidence has shown that the Yes-associated protein (YAP), the major effector of the Hippo pathway, can play a crucial role in pathogenesis and development of atherosclerosis. Activation of YAP-related pathways, which are induced by alerting flow pattern and matrix stiffness among others, can regulate processes including vascular endothelial cell dysfunction, monocyte infiltration, and smooth muscle cell migration, which contribute to atherosclerotic lesion formation. Further, YAP potentially modulates atherosclerotic complications such as vascular calcification and intraplaque hemorrhage, which require further investigation. Here, we summarized the relevant literature to outline current findings detailing the relationship between of YAP and atherosclerosis and highlight areas for future research.
Highlights
Atherosclerosis, a pathologic process underlying most cerebrovascular and cardiovascular diseases such as ischemic heart disease and stroke, remains a predominant cause of morbidity and mortality globally, carrying a considerable burden on public health [1, 2]
Xiao et al found that tissue factor pathway inhibitor-1 (TFPI-1) knockout in vascular smooth muscle cells (VSMCs) reduces interaction between TFPI-1 and AMOT, which led to a decrease in Yes-associated protein (YAP) phosphorylation, increasing nuclear translocation of YAP
YAP is a crucial transcriptional cofactor that is regulated by multiple stimuli and, mediates various pathways to initiate atherosclerosis development
Summary
Atherosclerosis, a pathologic process underlying most cerebrovascular and cardiovascular diseases such as ischemic heart disease and stroke, remains a predominant cause of morbidity and mortality globally, carrying a considerable burden on public health [1, 2]. Atherosclerosis is characterized by chronic inflammation in the arterial wall and, is triggered by endothelial cell dysfunction and structural alterations, including loss of the continuous luminal elastin layer and the exposure of proteoglycans [3]. This process, impairs the endothelial barrier and permits the subendothelial aggregation of low-density lipoprotein (LDL) to form asymmetric focal thickenings of the intima. Atherosclerotic lesions occur primarily in arterial branches, bifurcations, and curvatures, with uneven distribution of lesions throughout the vascular tree [5] This site-specificity gives rise to the hydromechanics effect on the pathogenesis of atherosclerosis, where blood flow-induced shear stress plays a vital role in determining where most vascular lesions originate. We review current findings to elucidate the role of YAP in atherosclerosis and related complications
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