Proinflammation: The key to arterial aging

Mingyi Wang, Liqun Jiang, Robert E. Monticone, Edward G. Lakatta

Research output: Contribution to journalReview article

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.

Original languageEnglish (US)
Pages (from-to)72-79
Number of pages8
JournalTrends in Endocrinology and Metabolism
Volume25
Issue number2
DOIs
StatePublished - Feb 1 2014
Externally publishedYes

Keywords

  • Angiotensin II
  • Atherosclerosis
  • Central arterial aging
  • Hypertension
  • Proinflammation

ASJC Scopus subject areas

  • Endocrinology, Diabetes and Metabolism
  • Endocrinology

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