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TAVI Represents an Anti-Inflammatory Therapy via Reduction of Shear Stress Induced, Piezo-1-Mediated Monocyte Activation Treatment Effects of Pulmonary Artery Denervation for Pulmonary Arterial Hypertension Stratified by REVEAL Risk Score: Results from PADN-CFDA Trial Hemodynamic, Functional, and Clinical Responses to Pulmonary Artery Denervation in Patients With Pulmonary Arterial Hypertension of Different Causes 3-Year Outcomes After 2-Stent With Provisional Stenting for Complex Bifurcation Lesions Defined by DEFINITION Criteria Clinical Impact of Residual Leaks Following Left Atrial Appendage Occlusion: Insights From the NCDR LAAO Registry Half-Dose Direct Oral Anticoagulation Versus Standard Antithrombotic Therapy After Left Atrial Appendage Occlusion Haemodynamic definitions and updated clinical classification of pulmonary hypertension A Score to Assess Mortality After Percutaneous Mitral Valve Repair Defining cardiovascular toxicities of cancer therapies: an International Cardio-Oncology Society (IC-OS) consensus statement Propensity-Matched 1-Year Outcomes Following Transcatheter Aortic Valve Replacement in Low-Risk Bicuspid and Tricuspid Patients
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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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