Oxidative Stress, Inflammation, and Vascular Aging in Hypertension
Age related decline in function is a physiological phenomenon occurring in all organ systems. However, acceleration and early occurrence of this process are observed in cardiovascular pathologies, including hypertension.1,2 In the vascular system, this is characterized by progressive pathological remodeling with stiffening,3 typically associated with extracellular matrix (ECM) alterations in collagen and elastin.4 This is, in part, dependent on cellular senescence and growth arrest.5 Although hypertension and atherosclerosis are associated with accumulation of cellular senescence markers in the vascular wall, these conditions are often associated with vascular dysfunction rather than simple loss of proliferative capacity.6 For example, risk factors for cardiovascular disease, such as hypertension, smoking, hyperlipidaemia, or diabetes mellitus are associated with accelerated decline of vascular function.2 This is why vascular age determination has been introduced in key clinical guidelines for cardiovascular prevention, to indicate to the patient how their lifestyle contributes to the acceleration of vascular function deterioration.7 Oxidative stress and inflammation, key mechanisms of endothelial dysfunction and arterial damage, link these risk factors to vascular disease, arterial stiffness, and aging. These underlie macro and microangiopathy, renal dysfunction, cardiac ischemia, and cognitive decline (Figure) Several novel pathways regulating these mechanisms of accelerated vascular aging have been elucidated in recent issues of Hypertension and are further discussed in the present Best Papers in Hypertension review. Figure. Central role of oxidative stress in accelerated vascular aging in hypertension. AT1R indicates angiotensin II receptor type 1; BH2, dihydrobiopterin; BH4, tetrahydrobiopterin; BMP, bone morphogenic protein; CypD, cyclophilin D; eNOS, endothelial NO synthase; ET1R, endothelin 1 receptor; H2O2, hydrogen peroxide; MMP, matrix metalloproteinase; Nox, NADPH oxidase; O2 superoxide anion; RANTES, regulated on activation, normal T cell expressed and secreted chemokine; and SmgGDS, GTP binding protein dissociation
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