Pathologic Cellular Events in Smoking-Related Pancreatitis

Cancers

Edwin Thrower¹ 

[1] Department of Internal Medicine, Section of Digestive Diseases, Yale University School of Medicine, New Haven, CT 06520, USA; E-Mail:

关键词: pancreatitis;    smoking;    nicotine;    4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK);    nicotinic acetylcholine receptors (nAChRs);    inflammation;    bioactivation;    β-adrenergic receptors;   

DOI  :  10.3390/cancers7020723

来源: mdpi

【 摘 要 】

Pancreatitis, a debilitating inflammatory disorder, results from pancreatic injury. Alcohol abuse is the foremost cause, although cigarette smoking has recently surfaced as a distinct risk factor. The mechanisms by which cigarette smoke and its toxins initiate pathological cellular events leading to pancreatitis, have not been clearly defined. Although cigarette smoke is composed of more than 4000 compounds, it is mainly nicotine and the tobacco-specific nitrosamine 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK), which have been extensively studied with respect to pancreatic diseases. This review summarizes these research findings and highlights cellular pathways which may be of relevance in initiation and progression of smoking-related pancreatitis.

【 授权许可】

CC BY   
© 2015 by the authors; licensee MDPI, Basel, Switzerland.