Multifaceted Mechanisms of Vascular Calcification in Aging

Author(s)

Pescatore, Luciana A. ^{[1, 2]} ; Gamarra, Lionel F. ^[2] ; Liberman, Marcel ^[2]

Affiliation

^[1] Univ Sao Paulo, Fac Med, Hosp Clin HCFMUSP, Lab Biol Vasc, Inst Coracao InCor, Sao Paulo, SP - Brazil

^[2] Hosp Israelita Albert Einstein, Avenida Albert Einstein 627, Floor 2SS, BR-05651 Sao Paulo, SP - Brazil

• Document type: Journal article
• Source: ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY; v. 39, n. 7, p. 1307-1316, JUL 2019.
• Web of Science Citations: 1

Abstract

Approximately 20% of the world's population will be around or above 65 years of age by the next decade. Out of these, 40% are suspected to have cardiovascular diseases as a cause of mortality. Arteriosclerosis, characterized by increased vascular calcification, impairing Windkessel effect and tissue perfusion, and determining end-organ damage, is a hallmark of vascular pathology in the elderly population. Risk factors accumulated during aging affect the normal physiological and vascular aging process, which contributes to the progression of arteriosclerosis. Traditional risk factors, age-associated diseases, and respective regulating mechanisms influencing vascular calcification and vascular stiffness have been extensively studied for many years. Despite the well-known fact that aging alone can induce vascular damage, specific mechanisms that implicate physiological aging in vascular calcification, contributing to vascular stiffness, are poorly understood. This review focuses on mechanisms activated during normal aging, for example, cellular senescence, autophagy, extracellular vesicles secretion, and oxidative stress, along with the convergence of premature aging models' pathophysiology, such as Hutchinson-Gilford Progeria (prelamin accumulation) and Klotho deficiency, to understand vascular calcification in aging. Understanding the mechanisms of vascular damage in aging that intersect with age-associated diseases and risk factors is crucial to foster innovative therapeutic targets to mitigate cardiovascular disease. (AU)

• FAPESP's process: 15/25923-0 - Modulation of vascular calcification by protein disulfide isomerase: study on a new transgenic mouse model
• Grantee: Luciana Pescatore Alves
• Support Opportunities: Scholarships in Brazil - Post-Doctoral
• FAPESP's process: 16/17961-1 - Role of gamma-carboxyglutamic protein functional imbalance in vascular calcification modulation of diabetic patients with peripheral arterial disease
• Grantee: Marcel Liberman
• Support Opportunities: Regular Research Grants
• FAPESP's process: 16/21470-3 - Therapeutic action of mesenchymal stem cells from human bone marrow labeled with multimodal nanoparticles in diabetic rats subjected to stroke: study of cellular, molecular and functional mechanisms.
• Grantee: Lionel Fernel Gamarra Contreras
• Support Opportunities: Regular Research Grants