Editorial: Vascular function and mechanisms of aging: hypertension, obesity and metabolic disorders

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Editorial on the Research Topic Vascular function and mechanisms of aging: hypertension, obesity and metabolic disordersWithin the context of age-related decline, quality of life is intensely affected by the functional deterioration of the cardiovascular system.Understanding the role of obesity, hypertension, and metabolic disorders on vascular function and subsequent vascular aging is crucial for clinical and basic research and raises a strong interest to the scientific community.Indeed, a quick search yielded 26,984 articles published in the PUBMED database with the terms "Vascular Function and Aging."Vascular aging is a multifactorial phenomenon that begins even before birth.However, we still do not have a single "true and complete" measure of this complex phenomenon; many parameters and tools have been proposed, all of which describe in a very fragmented way different aspects of the underlying process of "vascular aging" (Rietzschel and De Buyzere, 2022).Aging, hypertension, insulin resistance, obesity and atherosclerosis severely deteriorate the morphology and function of the cardiovascular system (Folkow and Svanborg, 1993;Küng and Lüscher, 1995).Blood vessels, specifically, show mechanical and morphological changes as well as endothelial and smooth muscle dysfunction (Ferrari et al., 2003).A decline in the distensibility of the aorta (Hallock and Benson, 1937) can be often detected in aging (Reddy et al., 2003).The morphological bases for these mechanical alterations are the vascular changes that take place during senescence.Arteries become elongated and tortuous presenting intimal and medial thickening as well as an increase in collagen accumulation in the media, and elastin fragmentation (Ferrari et al., 2003).Arterial stiffness is a marker of the interactions between hemodynamics and mechanosensing.Despite advances in studying age-induced arterial stiffness (Sehgel et al., 2015;Trache et al., 2020), there is a need to expand our understanding of the many steps involved in integrin-based adhesion and nucleo-cytoskeletal coupling, as well as mechanotransduction-regulated epigenetics (Lacolley et al., 2020).Importantly, aging causes a decay in endothelium-dependent relaxation both in animal models (Llorens et al., 2007) and humans (Egashira et al., 1993).Indeed, it can be stated that

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