General Mechanisms of Nicotine-induced Fibrogenesis

Overview

Journal FASEB J

Specialties Biology
Physiology

Date 2012 Aug 22

PMID 22906950

Citations 43

Authors

Kendal Jensen

Damir Nizamutdinov

Micheleine Guerrier

Syeda Afroze

David Dostal

Shannon Glaser

Affiliations

Soon will be listed here.

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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