Abstract
The incidence of stroke and myocardial infarction increases in aged patients and it is associated with an adverse outcome. Considering the aging population and the increasing incidence of cardiovascular disease, the prediction for population well-being and health economics is daunting. Accordingly, there is an unmet need to focus on fundamental processes underlying vascular aging. A better understanding of the pathways leading to arterial aging may contribute to design mechanism-based therapeutic approaches to prevent or attenuate features of vascular senescence. In the present review, we discuss advances in the pathophysiology of age-related vascular dysfunction including nitric oxide signalling, dysregulation of oxidant/inflammatory genes, epigenetic modifications and mechanisms of vascular calcification as well as insights into vascular repair. Such an overview highlights attractive molecular targets for the prevention of age-driven vascular disease.
- arterial aging
- inflammation
- oxidative stress
- pathways
- vascular repair
Abbreviations: ALDH2, aldehyde dehydrogenase 2; AMPK, AMP-activated protein kinase; AP-1, activated protein 1; ApoE, apolipoprotein E; Arg II, arginase II; BAP, bone alkaline phosphatase; BH4, tetrahydrobiopterin; CV, cardiovascular; CVD, cardiovascular disease; eNOS, endothelial nitric oxide synthase; EOC, early angiogenic outgrowth cell; EPC, endothelial progenitor cell; fOXO, Forkhead box O; HIF-1α, hypoxia inducible factor 1α; MCC, myeloid calcifying cell; NF-κB, nuclear factor κB; OC, osteocalcin; PI3K, phosphoinositide 3-kinase; RANKL, receptor activator of NF-κB ligand; ROS, reactive oxygen species; SDF-1, stromal cell-derived factor 1; VSMC, vascular smooth muscle cell; WT, wild-type
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