CBS 2019
CBSMD教育中心
English

科学研究

科研文章

荐读文献

Definitions and classifications of bifurcation lesions and treatment Propensity-Matched 1-Year Outcomes Following Transcatheter Aortic Valve Replacement in Low-Risk Bicuspid and Tricuspid Patients Defining cardiovascular toxicities of cancer therapies: an International Cardio-Oncology Society (IC-OS) consensus statement Beta-Blockers after Myocardial Infarction and Preserved Ejection Fraction Definition, classification and diagnosis of pulmonary hypertension Beta-Blockers after Myocardial Infarction and Preserved Ejection Fraction Viridans Streptococcal Biofilm Evades Immune Detection and Contributes to Inflammation and Rupture of Atherosclerotic Plaques Homocysteine metabolism as the target for predictive medical approach, disease prevention, prognosis, and treatments tailored to the person Endothelial ACKR3 drives atherosclerosis by promoting immune cell adhesion to vascular endothelium TRAP1 drives smooth muscle cell senescence and promotes atherosclerosis via HDAC3-primed histone H4 lysine 12 lactylation

Review ArticleVolume 75, Issue 8, March 2020

JOURNAL:J Am Coll Cardiol. Article Link

Mechanisms of Vascular Aging, A Geroscience Perspective JACC Focus Seminar

Z Ungvari, S Tarantini, F Sorond et al. Keywords: atherosclerosis; endothelial dysfunction; geroscience; microcirculation; senescence

ABSTRACT

Age-related pathological alterations of the vasculature have a critical role in morbidity and mortality of older adults. In epidemiological studies, age is the single most important cardiovascular risk factor that dwarfs the impact of traditional risk factors. To develop novel therapeutic interventions for prevention of age-related vascular pathologies, it is crucial to understand the cellular and molecular mechanisms of vascular aging. In this review, shared molecular mechanisms of aging are considered in terms of their contribution to the pathogenesis of macrovascular and microvascular diseases associated with old age. The role of cellular senescence in development of vascular aging phenotypes is highlighted, and potential interventions to prevent senescence and to eliminate senescent cells for prevention of vascular pathologies are presented. The evidence supporting a role for interorgan communication and circulating progeronic and antigeronic factors in vascular aging is discussed.