The increasing mean age of the population in developed countries has turned out to be an economic and social problem. Cardiovascular disease has long been considered to be age related in terms of their onset and progression. As such, we can say that the increase in life expectancy goes in parallel with increased incidence of cardiovascular disease. With age, a number of changes occur in the vasculature altering the homeostasis of the irrigated organs promoting target organ damage. While different adaptive mechanisms to protect vessels against mild stress have been described, the aging process induces a progressive failure of protective mechanisms, leading to vascular changes and higher susceptibility to cardiovascular diseases. Indeed, vascular aging is exacerbated by coexisting cardiovascular risk factors, such as hypertension, metabolic syndrome and diabetes.
Compelling evidence indicates that diminished endothelial relaxation and increase, decrease, or no change in contractile responses to several agonists is associated with aging. There is an increase of vasoconstrictor factors expression and a decrease of vasodilators. Morphologic changes include lumen diameter enlargement, wall thickening and alterations of matrix substances as increased collagen or decreased elastin deposition, ultimately leading to greater arterial stiffening (reduced compliance). Importantly, arterial stiffness is an independent predictor of cardiovascular morbidity and mortality. Cellular and molecular mechanisms have also been documented. Senescence at the cellular level involves alterations in Ca2+ signaling and down regulation of anti-aging proteins. Both endothelial and smooth muscle cells change their number, morphology, function and their regenerative ability. Aging is also associated with a gradual loss of antioxidant defense mechanisms, a proinflammatory shift in the cytokine expression profile and a production of reactive oxygen species such as superoxide (O2-) that promotes the breakdown of nitric oxide. Nitric oxide and O2- interact to form peroxynitrite known to nitrosylate proteins affecting their physiological function. However, vascular wall proteins may also suffer from other potentially deleterious modifications as glycation (Maillard reaction) and glyco-oxidative reactions with increasing age, which could be linked to the age-associated changes in vascular function.
Various strategies have shown benefit in preventing, delaying or attenuating vascular aging. For instance, a healthy lifestyle including low fat diet and/or exercise have a favorable effect. Nevertheless, it yet remains to be fully demonstrated whether vascular aging can be pharmacologically prevented. This Research Topic is intended to bring together research efforts to understand the causes and consequences of vascular aging and propose new therapeutic strategies for the management of vascular senescence.
The increasing mean age of the population in developed countries has turned out to be an economic and social problem. Cardiovascular disease has long been considered to be age related in terms of their onset and progression. As such, we can say that the increase in life expectancy goes in parallel with increased incidence of cardiovascular disease. With age, a number of changes occur in the vasculature altering the homeostasis of the irrigated organs promoting target organ damage. While different adaptive mechanisms to protect vessels against mild stress have been described, the aging process induces a progressive failure of protective mechanisms, leading to vascular changes and higher susceptibility to cardiovascular diseases. Indeed, vascular aging is exacerbated by coexisting cardiovascular risk factors, such as hypertension, metabolic syndrome and diabetes.
Compelling evidence indicates that diminished endothelial relaxation and increase, decrease, or no change in contractile responses to several agonists is associated with aging. There is an increase of vasoconstrictor factors expression and a decrease of vasodilators. Morphologic changes include lumen diameter enlargement, wall thickening and alterations of matrix substances as increased collagen or decreased elastin deposition, ultimately leading to greater arterial stiffening (reduced compliance). Importantly, arterial stiffness is an independent predictor of cardiovascular morbidity and mortality. Cellular and molecular mechanisms have also been documented. Senescence at the cellular level involves alterations in Ca2+ signaling and down regulation of anti-aging proteins. Both endothelial and smooth muscle cells change their number, morphology, function and their regenerative ability. Aging is also associated with a gradual loss of antioxidant defense mechanisms, a proinflammatory shift in the cytokine expression profile and a production of reactive oxygen species such as superoxide (O2-) that promotes the breakdown of nitric oxide. Nitric oxide and O2- interact to form peroxynitrite known to nitrosylate proteins affecting their physiological function. However, vascular wall proteins may also suffer from other potentially deleterious modifications as glycation (Maillard reaction) and glyco-oxidative reactions with increasing age, which could be linked to the age-associated changes in vascular function.
Various strategies have shown benefit in preventing, delaying or attenuating vascular aging. For instance, a healthy lifestyle including low fat diet and/or exercise have a favorable effect. Nevertheless, it yet remains to be fully demonstrated whether vascular aging can be pharmacologically prevented. This Research Topic is intended to bring together research efforts to understand the causes and consequences of vascular aging and propose new therapeutic strategies for the management of vascular senescence.
