TY - CHAP M1 - Book, Section TI - Cardiovascular Disease and Ageing: Cellular and Molecular Mechanisms A1 - Ungvari, Zoltan A1 - Dai, Dao-Fu A1 - Merkely, Bela A1 - Csiszar, Anna A2 - Fuster, Valentin A2 - Narula, Jagat A2 - Vaishnava, Prashant A2 - Leon, Martin B. A2 - Callans, David J. A2 - Rumsfeld, John S. A2 - Poppas, Athena Y1 - 2022 N1 - T2 - Fuster and Hurst's The Heart, 15e AB - Chapter SummaryThis chapter discusses the pathophysiology of the aging processes in relation to the cardiovascular system. Epidemiological studies demonstrate that the impact of conventional cardiovascular risk factors (eg, diabetes, hypertension, dyslipidemia, lifestyle factors, etc.) on the prevalence of cardiovascular and cerebrovascular diseases are dwarfed by the magnitude of effect of advanced aging in relation to these diseases. Both cell autonomous and cell nonautonomous mechanisms of aging contribute to the pathogenesis of these diseases, including age-related oxidative stress, mitochondrial dysfunction, NAD+ depletion and dysregulation of sirtuin-regulated pathways, impaired proteostasis and autophagy, low-grade sterile inflammation, and cellular senescence (see Fuster and Hurst’s Central Illustration). Emerging experimental evidence also supports the existence and significance of diverse secreted/circulatory factors derived from distal organs that modulate cardiac and vascular aging processes (including endocrine regulation). Emerging understanding of cardiac and vascular aging processes can enable the identification of novel targets for therapeutic intervention to reverse the deleterious consequences of cardiovascular aging and to improve cardiovascular and cerebrovascular health in older adults. SN - PB - McGraw-Hill Education CY - New York, NY Y2 - 2024/03/28 UR - accessmedicine.mhmedical.com/content.aspx?aid=1202453983 ER -