Reviewing Mechanisms of Vascular Aging

This review paper, like many, is largely concerned with the layer of aging biochemistry that involves changes in gene expression and functional alterations in cell behavior that can be attributed to those changes. This is a downstream area of the biochemistry of aging, very complex, caused by simpler forms of underlying molecular damage. That damage should be the primary target for research and development, not the consequences of damage.

It is possible to produce compensatory therapies that attempt to force a reversal in the age-related change in expression of specific genes, but this will never be anywhere near as effective an approach as targeting the underlying causes. One root cause form of molecular damage will result in countless gene expression and functional changes. Every one of those changes is a major research project, in the way that most new medical technology is presently developed. It would be far better to go after the root causes, and thus address many downstream consequences with a single major research project.

Vascular aging is an independent risk factor for morbidity and mortality of age-related diseases, particularly cardiovascular diseases (CVDs) such as hypertension and atherosclerosis. Vascular aging is characterized by vascular stiffening, intimal and medial thickening, increased luminal diameter, reorganization of the extracellular matrix, and endothelial dysfunction. The theories for the mechanisms of vascular aging include inflammation, mitochondrial dysfunction, oxidative stress, telomere attrition, epigenetics, and autophagy.

Inflammaging occurs during physiological aging in the absence of an overt infection, which describes the low-grade, chronic systemic inflammation. Inflammaging plays a role in all age-related diseases such as CVDs, which affect the mortality and morbidity of elderly people. The activation of immune cells such as macrophages / monocytes and the endothelial cell dysfunction participates in vascular low-grade inflammatory processes.

Growing research has identified that hypoxia-inducible factor-1α (HIF-1α) has an important effect on the aging-related process, particularly regulating cardiovascular aging. Vascular endothelial growth factor (VEGF), which is regulated by HIF-1, is a significant regulator for angiogenesis and a vital player of vascular aging. The activity of HIF-1 decreases during aging and then downregulates the expression of VEGF and results in the impairment of angiogenesis. The research found that HIF-1α is involved in regulating vascular inflammation in macrophages by limiting excessive vascular remodeling. In conclusion, HIF-1α may be a potential therapeutic target in vascular diseases, particularly in vascular aging.


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