Abstract

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.

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Publisher Full Text

Authors

Jensen K, Nizamutdinov D, Guerrier M, Afroze S, Dostal D, Glaser S

Institution

Division of Gastroenterology, Texas A&M Health Science Center, Central Texas Veterans Health Care System, 1901 South 1st St., Temple, TX 76504, USA.

Source

FASEB journal : official publication of the Federation of American Societies for Experimental Biology 26:12 2012 Dec pg 4778-87

MeSH

Epithelial Cells
Fibrosis
Ganglionic Stimulants
Humans
Kidney
Liver
Lung
Neoplasms
Nicotine
Transforming Growth Factor beta1

Pub Type(s)

Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, Non-P.H.S.
Review

Language

eng

PubMed ID

22906950