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动脉粥样硬化性心血管疾病

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Machine Learning Using CT-FFR Predicts Proximal Atherosclerotic Plaque Formation Associated With LAD Myocardial Bridging Active factor XI is associated with the risk of cardiovascular events in stable coronary artery disease patients Parallel Murine and Human Plaque Proteomics Reveals Pathways of Plaque Rupture Apolipoprotein A-V is a potential target for treating coronary artery disease: evidence from genetic and metabolomic analyses Independent Association of Lipoprotein(a) and Coronary Artery Calcification With Atherosclerotic Cardiovascular Risk Comprehensive Management of Cardiovascular Risk Factors for Adults With Type 2 Diabetes: A Scientific Statement From the American Heart Association Potential Mechanisms of In-stent Neointimal Atherosclerotic Plaque Formation Autologous CD34+ Stem Cell Therapy Increases Coronary Flow Reserve and Reduces Angina in Patients With Coronary Microvascular Dysfunction Cardiovascular risk prediction in type 2 diabetes: a comparison of 22 risk scores in primary care settings Nicotine promotes vascular calcification via intracellular Ca21-mediated, Nox5-induced oxidative stress, and extracellular vesicle release in vascular smooth muscle cells
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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.
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