Aging-Induced Impairment of Vascular Function: Mitochondrial Redox Contributions and Physiological/Clinical Implications

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

• Level A · Stronger Clinical Evidence
• Level B · Emerging clinical evidence with positive signals
• Level C · Early human research exploring benefits
• Level D · Scientific groundwork from lab and animal studies
• Emerging · Emerging topic under active research

Abstract (original English)

Significance: The vasculature responds to the respiratory needs of tissue by modulating luminal diameter through smooth muscle constriction or relaxation. Coronary perfusion, diastolic function, and coronary flow reserve are drastically reduced with aging. This loss of blood flow contributes to and exacerbates pathological processes such as angina pectoris, atherosclerosis, and coronary artery and microvascular disease. Recent Advances: Increased attention has recently been given to defining mechanisms behind aging-mediated loss of vascular function and development of therapeutic strategies to restore youthful vascular responsiveness. The ultimate goal aims at providing new avenues for symptom management, reversal of tissue damage, and preventing or delaying of aging-induced vascular damage and dysfunction in the first place. Critical Issues: Our major objective is to describe how aging-associated mitochondrial dysfunction contributes to endothelial and smooth muscle dysfunction via dysregulated reactive oxygen species production, the clinical impact of this phenomenon, and to discuss emerging therapeutic strategies. Pathological changes in regulation of mitochondrial oxidative and nitrosative balance (Section 1) and mitochondrial dynamics of fission/fusion (Section 2) have widespread effects on the mechanisms underlying the ability of the vasculature to relax, leading to hyper

Evidence level

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

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