Open AccessInflammation and endothelial dysfunction during aging: role of NF-κB
Author(s) -
Anna Csiszár,
Mingyi Wang,
Edward G. Lakatta,
Zoltán Ungvári
Publication year - 2008
Publication title -
journal of applied physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.253
H-Index - 229
eISSN - 8750-7587
pISSN - 1522-1601
DOI - 10.1152/japplphysiol.90470.2008
Subject(s) - inflammation , oxidative stress , endothelial dysfunction , proinflammatory cytokine , biology , pathogenesis , nf κb , angiotensin ii , tumor necrosis factor alpha , nfkb1 , endothelial activation , signal transduction , immunology , microbiology and biotechnology , endocrinology , transcription factor , biochemistry , blood pressure , gene
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-alpha-converting enzyme (TACE)-TNF-alpha, and the renin-angiotensin system may underlie NF-kappaB induction and endothelial activation in aged arteries. The theme that emerges from this review is that multiple proinflammatory pathways converge on NF-kappaB in the aged arterial wall, and that the transcriptional activity of NF-kappaB 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-kappaB activity in endothelial cells.