Mechanisms of endothelial senescence and vascular aging

Abstract

Scope: Cardiovascular disease (CVD) is a major cause of mortality, especially in the aging population. Aging is one of the main risk factors contributing to CVD, leading to early mortality and a decline in the quality of life. Vascular aging is closely linked with atherosclerosis, diabetes, hypertension, stroke, heart failure, and peripheral arterial diseases. Elucidating the cellular and molecular mechanisms underlying vascular aging help to develop therapeutic strategies that can address age-related vascular diseases and decrease the rate of morbidity and mortality among the older population. Endothelial cells located on the interior layer of blood vessels. Intima layers of vascular vessels are damaged and remodeled during vascular aging. The dysfunction of smooth muscle cells and endothelial cells plays key roles in vascular aging. Common pathological changes during vascular aging include arterial stiffness, calcification, and atherosclerosis. Endothelial cell senescence is driven by complex underlying mechanisms. The complex regulation of aging and antiaging network in endothelial cells involve several factors, such as Klotho protein, nitric oxide, fibroblast growth factor 21 (FGF21), and SIRT family members.

Objectives: This review aims to systematically delineate the mechanisms underlying the endothelial senescence.

Methodology: The publications on the endothelial cell senescence mechanisms and its roles in vascular aging and aging related diseases are comprehensively investigated and summarized. In this review, the roles of various components in endothelial cell senescence are discussed to elucidate the underlying molecular mechanisms of endothelial cell senescence and identify potential therapeutic targets.

Keywords: Autophagy; Endothelial senescence; Inflammation; Mitochondria; ROS; Vascular aging.