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Trends Endocrinol Metab. 2014 Feb;25(2):72-9. doi: 10.1016/j.tem.2013.10.002. Epub 2013 Dec 20.

Proinflammation: the key to arterial aging.

Author information

1
Laboratory of Cardiovascular Science, National Institution on Aging, National Institutes of Health, Biomedical Research Center (BRC), 251 Bayview Boulevard, Baltimore, MD 21224, USA. Electronic address: mingyiw@grc.nia.nih.gov.
2
Laboratory of Cardiovascular Science, National Institution on Aging, National Institutes of Health, Biomedical Research Center (BRC), 251 Bayview Boulevard, Baltimore, MD 21224, USA.
3
Laboratory of Cardiovascular Science, National Institution on Aging, National Institutes of Health, Biomedical Research Center (BRC), 251 Bayview Boulevard, Baltimore, MD 21224, USA. Electronic address: lakattae@grc.nia.nih.gov.

Abstract

Arterial aging is the major contributing factor to increases in the incidence and prevalence of cardiovascular disease, due mainly to the presence of chronic, low-grade, 'sterile' arterial inflammation. Inflammatory signaling driven by the angiotensin II cascade perpetrates adverse age-associated arterial structural and functional remodeling. The aged artery is characterized by endothelial disruption, enhanced vascular smooth muscle cell (VMSC) migration and proliferation, extracellular matrix (ECM) deposition, elastin fracture, and matrix calcification/amyloidosis/glycation. Importantly, the molecular mechanisms of arterial aging are also relevant to the pathogenesis of hypertension and atherosclerosis. Age-associated arterial proinflammation is to some extent mutable, and interventions to suppress or delay it may have the potential to ameliorate or retard age-associated arterial diseases.

KEYWORDS:

angiotensin II; atherosclerosis; central arterial aging; hypertension; proinflammation

PMID:
24365513
PMCID:
PMC3917314
DOI:
10.1016/j.tem.2013.10.002
[Indexed for MEDLINE]
Free PMC Article
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