The DOI matches its Crossref record; 9 of the 9 references it cites were found in a registry or an index.
Vasoprotective effects of resveratrol and SIRT1: attenuation of cigarette smoke-induced oxidative stress and proinflammatory phenotypic alterations
Open accessAbstract
The dietary polyphenolic compound resveratrol, by activating the protein deacetylase enzyme silent information regulator 2/sirtuin 1 (SIRT1), prolongs life span in evolutionarily distant organisms and may mimic the cytoprotective effects of dietary restriction. The present study was designed to elucidate the effects of resveratrol on cigarette smoke-induced vascular oxidative stress and inflammation, which is a clinically highly relevant model of accelerated vascular aging. Cigarette smoke exposure of rats impaired the acetylcholine-induced relaxation of carotid arteries, which could be prevented by resveratrol treatment. Smoking and in vitro treatment with cigarette smoke extract (CSE) increased reactive oxygen species production in rat arteries and cultured coronary arterial endothelial cells (CAECs), respectively, which was attenuated by resveratrol treatment. The smoking-induced upregulation of inflammatory markers (ICAM-1, inducible nitric oxide synthase, IL-6, and TNF-α) in rat arteries was also abrogated by resveratrol treatment. Resveratrol also inhibited CSE-induced NF-κB activation and inflammatory gene expression in CAECs. In CAECs, the aforementioned protective effects of resveratrol were abolished by knockdown of SIRT1, whereas the overexpression of SIRT1 mimicked the effects of resveratrol. Resveratrol treatment of rats protected aortic endothelial cells against cigarette smoking-induced apoptotic cell death. Resveratrol also exerted antiapoptotic effects in CSE-treated CAECs, which could be abrogated by knockdown of SIRT1. Resveratrol treatment also attenuated CSE-induced DNA damage in CAECs (comet assay). Thus resveratrol and SIRT1 exert antioxidant, anti-inflammatory, and antiapoptotic effects, which protect the endothelial cells against the adverse effects of cigarette smoking-induced oxidative stress. The vasoprotective effects of resveratrol will likely contribute to its antiaging action in mammals and may be especially beneficial in pathophysiological conditions associated with accelerated vascular aging.
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Cites
Resveratrol improves health and survival of mice on a high-calorie diet
Baur, J. A., Pearson, K. J., Price, N. L., Jamieson, H. A., Lerin, C., Kalra, A., Prabhu, V. V., Allard, J. S., Lopez-Lluch, G., Lewis, K., et al. (2006) · Nature · doi:10.1038/nature05354 · Cited by 4,290
Small molecule activators of sirtuins extend Saccharomyces cerevisiae lifespan
Howitz, K. T., Bitterman, K. J., Cohen, H. Y., Lamming, D. W., Lavu, S., Wood, J. G., Zipkin, R. E., Chung, P., Kisielewski, A., Zhang, L.-L., et al. (2003) · Nature · doi:10.1038/nature01960 · Cited by 3,796
Modulation of NF‐κB‐dependent transcription and cell survival by the SIRT1 deacetylase
Yeung, F., Hoberg, J. E., Ramsey, C. S., Keller, M. D., Jones, D. R., Frye, R. A., & Mayo, M. W. (2004) · The EMBO Journal · doi:10.1038/sj.emboj.7600244 · Cited by 2,750
The pathophysiology of cigarette smoking and cardiovascular disease
Ambrose, J. A., & Barua, R. S. (2004) · Journal of the American College of Cardiology · doi:10.1016/j.jacc.2003.12.047 · Cited by 2,394
Sirtuin activators mimic caloric restriction and delay ageing in metazoans
Wood, J. G., Rogina, B., Lavu, S., Howitz, K., Helfand, S. L., Tatar, M., & Sinclair, D. (2004) · Nature · doi:10.1038/nature02789 · Cited by 1,868
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Xanthine Oxidase Inhibition Reverses Endothelial Dysfunction in Heavy Smokers
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“In this regard, a recent study demonstrated that acrolein, a major toxicant in cigarette smoke, causes oxidative mitochondrial damage (36).”
BackgroundMendelson, J. H., Sholar, M. B., Mutschler, N. H., Jaszyna-Gasior, M., Goletiani, N. V., Siegel, A. J., & Mello, N. K. (2003) · The Journal of Pharmacology and Experimental Therapeutics · doi:10.1124/jpet.103.052928 · Cited by 81
Cited by
Mammalian Sirtuins: Biological Insights and Disease Relevance
Haigis, M. C., & Sinclair, D. A. (2010) · Annual Review of Pathology: Mechanisms of Disease · doi:10.1146/annurev.pathol.4.110807.092250 · Cited by 2,085
Endothelial dysfunction and vascular disease - a 30th anniversary update
Vanhoutte, P. M., Shimokawa, H., Feletou, M., & Tang, E. H. C. (2017) · Acta Physiologica · doi:10.1111/apha.12646 · Cited by 937
Redox regulation of SIRT1 in inflammation and cellular senescence
Hwang, J.-W., Yao, H., Caito, S., Sundar, I. K., & Rahman, I. (2013) · Free Radical Biology and Medicine · doi:10.1016/j.freeradbiomed.2013.03.015 · Cited by 503
Inflammation and endothelial dysfunction during aging: role of NF-κB
Csiszar, A., Wang, M., Lakatta, E. G., & Ungvari, Z. (2008) · Journal of Applied Physiology · doi:10.1152/japplphysiol.90470.2008 · Cited by 441
Self-citationNegative regulation of inflammation by SIRT1
Xie, J., Zhang, X., & Zhang, L. (2013) · Pharmacological Research · doi:10.1016/j.phrs.2012.10.010 · Cited by 234
Metadata
- Authors
- Csiszar, A., Labinskyy, N., Podlutsky, A., Kaminski, P. M., Wolin, M. S., Zhang, C., Mukhopadhyay, P., Pacher, P., Hu, F., de Cabo, R., Ballabh, P., & Ungvari, Z.
- Venue
- American Journal of Physiology-Heart and Circulatory Physiology
- Publisher
- American Physiological Society
- Published
- 2008-06
- Volume
- 294
- Issue
- 6
- Pages
- H2721-H2735
- ISSN
- 0363-6135 (ISSN-L)
- 1522-1539
- OpenAlex
- W2125114619
- Cited by
- 276
- References
- 9
- FWCI
- 9.87
- Type
- journal article
- Language
- en
- Open access
- green
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