Aging of Vascular System Is a Complex Process: The Cornerstone Mechanisms

Abstract

Aging is one of the most intriguing processes of human ontogenesis. It is associated with the development of a wide variety of diseases affecting all organs and their systems. The victory over aging is the most desired goal of scientists; however, it is hardly achievable in the foreseeable future due to the complexity and ambiguity of the process itself. All body systems age, lose their performance, and structural disorders accumulate. The cardiovascular system is no exception. And it is cardiovascular diseases that occupy a leading position as a cause of death, especially among the elderly. The aging of the cardiovascular system is well described from a mechanical point of view. Moreover, it is known that at the cellular level, a huge number of mechanisms are involved in this process, from mitochondrial dysfunction to inflammation. It is on these mechanisms, as well as the potential for taking control of the aging of the cardiovascular system, that we focused on in this review.

Endogenous sulfur dioxide deficiency as a driver of cardiomyocyte senescence through abolishing sulphenylation of STAT3 at cysteine 259

“…The typical characteristics of cardiac aging are mainly composed with complex ventricular and valvular changes, including left ventricular hypertrophy, cardiac dysfunction, valvular degeneration, fibrosis, and decreased maximal exercise capacity [ [33] , [34] , [35] ], These changes can lead to cardiovascular diseases, including heart failure, atrial fibrillation, left ventricular hypertrophy, coronary artery disease, arrhythmias, and microcirculatory dysfunction in the older adult population [ 33 , 34 , 36 ]. Cardiac aging in mice is similar to that in humans and includes cardiac hypertrophy, fibrosis, dysfunction, as well as reduced functional reserve and resilience to stress [ 37 , 38 ].…”

Disparate Roles of Oxidative Stress in Rostral Ventrolateral Medulla in Age-Dependent Susceptibility to Hypertension Induced by Systemic l-NAME Treatment in Rats

“…The prevalence of hypertension increases markedly with aging, attributed primarily to alterations in the structure, responsiveness, function, and rigidity of vessel walls [ 35 ], as well as dysregulation of the autonomic nervous system [ 36 ]. Several theories have so far been proposed to explain the etiology of biological aging [ 37 ]; among them, tissue oxidative stress was postulated to be a common denominator [ 38 ]. Indeed, a wide array of studies suggests the engagement of ROS in age-related CVDs, including hypertension, atherosclerosis, atrial fibrillation, and stroke [ 38 ].…”