Multifaceted Mechanisms of Vascular Calcification in Aging

Autor(es)

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

Afiliação do(s) autor(es)

^[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

• Tipo de documento: Artigo Científico
• Fonte: ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY; v. 39, n. 7, p. 1307-1316, JUL 2019.
• Citações Web of Science: 1

Resumo

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)

• Processo FAPESP: 15/25923-0 - Modulação da calcificação vascular pela dissulfeto isomerase proteica (PDI): estudo em um novo modelo de camundongo transgênico
• Beneficiário: Luciana Pescatore Alves
• Modalidade de apoio: Bolsas no Brasil - Pós-Doutorado
• Processo FAPESP: 16/17961-1 - Investigação do desequilíbrio funcional da proteína glutâmica de matriz na modulação da calcificação vascular em pacientes diabéticos com doença arterial periférica
• Beneficiário: Marcel Liberman
• Modalidade de apoio: Auxílio à Pesquisa - Regular
• Processo FAPESP: 16/21470-3 - Ação terapêutica das células tronco mesenquimais da medula humana, marcadas com nanopartículas multimodais em ratos diabéticos submetidos a isquemia cerebral focal: estudo dos mecanismos celulares, moleculares e funcionais.
• Beneficiário: Lionel Fernel Gamarra Contreras
• Modalidade de apoio: Auxílio à Pesquisa - Regular