Inflammation and endothelial dysfunction during aging: Role of NF-κB

Anna Csiszar, Mingyi Wang, Edward G. Lakatta, Zoltan Ungvari

Research output: Contribution to journalReview article

Abstract

One of the major conceptual advances in our understanding of the pathogenesis of age-associated cardiovascular diseases has been the insight that age-related oxidative stress may promote vascular inflammation even in the absence of traditional risk factors associated with atherogenesis (e.g., hypertension or metabolic diseases). In the present review we summarize recent experimental data suggesting that mitochondrial production of reactive oxygen species, innate immunity, the local TNF-α-converting enzyme (TACE)-TNF-α, and the renin-angiotensin system may underlie NF-κB induction and endothelial activation in aged arteries. The theme that emerges from this review is that multiple proinflammatory pathways converge on NF-κB in the aged arterial wall, and that the transcriptional activity of NF-κB is regulated by multiple nuclear factors during aging, including nuclear enzymes poly(ADP-ribose) polymerase (PARP-1) and SIRT-1. We also discuss the possibility that nucleophosmin (NPM or nuclear phosphoprotein B23), a known modulator of the cellular oxidative stress response, may also regulate NF-κB activity in endothelial cells.

Original languageEnglish (US)
Pages (from-to)1333-1341
Number of pages9
JournalJournal of applied physiology
Volume105
Issue number4
DOIs
StatePublished - Oct 2008

Keywords

  • Caloric restriction
  • Coronary artery disease
  • Myocardial infarction
  • Poly(ADP-ribose) polymerase
  • Renin-angiotensin system
  • Resveratrol
  • Senescence
  • Stroke

ASJC Scopus subject areas

  • Physiology
  • Physiology (medical)

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