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Review article

Molecular pathways of arterial aging

Francesco Paneni, Sarah Costantino, Francesco Cosentino
Clinical Science Jan 01, 2015, 128 (2) 69-79; DOI: 10.1042/CS20140302
Francesco Paneni
Cardiology Unit, Department of Medicine, Karolinska University Hospital, Stockholm, Sweden
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Sarah Costantino
Cardiology Unit, Department of Medicine, Karolinska University Hospital, Stockholm, Sweden
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Francesco Cosentino
Cardiology Unit, Department of Medicine, Karolinska University Hospital, Stockholm, Sweden
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  • For correspondence: francesco.cosentino@ki.se
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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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January 2015

Volume: 128 Issue: 2

Clinical Science: 128 (2)
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Molecular pathways of arterial aging
Francesco Paneni, Sarah Costantino, Francesco Cosentino
Clinical Science Jan 2015, 128 (2) 69-79; DOI: 10.1042/CS20140302
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Molecular pathways of arterial aging
Francesco Paneni, Sarah Costantino, Francesco Cosentino
Clinical Science Jan 2015, 128 (2) 69-79; DOI: 10.1042/CS20140302

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  • Article
    • Abstract
    • AGING AND CARDIOVASCULAR DISEASE
    • STRUCTURAL ABNORMALITIES OF ARTERIAL AGING
    • NITRIC OXIDE SIGNALLING
    • OXIDATIVE STRESS
    • INFLAMMATION
    • ROLE AND MOLECULAR TARGETS OF SIRTUINS IN THE AGED VASCULATURE
    • ECTOPIC VASCULAR CALCIFICATION
    • AGE-DEPENDENT DECLINE OF VASCULAR HEALING PROCESS: CELLULAR AND MOLECULAR TARGETS
    • CONCLUSIONS
    • FUNDING
    • References
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Keywords

arterial aging
inflammation
oxidative stress
pathways
vascular repair

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