Journal
FASEB JOURNAL
Volume 26, Issue 12, Pages 4778-4787Publisher
FEDERATION AMER SOC EXP BIOL
DOI: 10.1096/fj.12-206458
Keywords
cigarette smoking; fibroblast; reactive oxygen species; collagen; NRT
Categories
Funding
- Scott and White Hospital, Department of Internal Medicine
- Scott and White Research Advancement award
- U.S. Department of Veteran's Affairs Career Development Award-2
- U.S. National Institutes of Health [DK081442]
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Cigarette smoking contributes to the development of cancer, and pathogenesis of other diseases. Many chemicals have been identified in cigarettes that have potent biological properties. Nicotine is especially known for its role in addiction and plays a role in other physiological effects of smoking and tobacco use. Recent studies have provided compelling evidence that, in addition to promoting cancer, nicotine also plays a pathogenic role in systems, such as the lung, kidney, heart, and liver. In many organ systems, nicotine modulates fibrosis by altering the functions of fibroblasts. Understanding the processes modulated by nicotine holds therapeutic potential and may guide future clinical and research decisions. This review discusses the role of nicotine in the general fibrogenic process that governs fibrosis and fibrosis-related diseases, focusing on the cellular mechanisms that have implications in multiple organ systems. Potential research directions for the management of nicotine-induced fibrosis, and potential clinical considerations with regard to nicotine-replacement therapy (NRT) are presented.-Jensen, K., Nizamutdinov, D., Guerrier, M., Afroze, S., Dostal, D., Glaser, S. General mechanisms of nicotine-induced fibrogenesis. FASEB J. 26, 4778-4787 (2012). www.fasebj.org
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