期刊
JOURNAL OF APPLIED PHYSIOLOGY
卷 105, 期 4, 页码 1333-1341出版社
AMER PHYSIOLOGICAL SOC
DOI: 10.1152/japplphysiol.90470.2008
关键词
senescence; resveratrol; caloric restriction; poly(ADP-ribose) polymerase; renin-angiotensin system; coronary artery disease; stroke; myocardial infarction
资金
- National Institute on Aging
- American Heart Association [0430108N, 0435140N]
- National Institutes of Health [HL-077256, HL-43023]
- American Diabetes Association, American Federation for Aging Researc
- Philip Morris International
- NATIONAL HEART, LUNG, AND BLOOD INSTITUTE [R01HL077256, P01HL043023] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE ON AGING [Z01AG000237] Funding Source: NIH RePORTER
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-kappa B induction and endothelial activation in aged arteries. The theme that emerges from this review is that multiple proinflammatory pathways converge on NF-kappa B in the aged arterial wall, and that the transcriptional activity of NF-kappa B 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-kappa B activity in endothelial cells.
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