Manohar M, Verma AK, Venkateshaiah SU, Sanders NL, Mishra A. Pathogenic mechanisms of pancreatitis. World J Gastrointest Pharmacol Ther 2017; 8(1): 10-25 [PMID: 28217371 DOI: 10.4292/wjgpt.v8.i1.10]
Corresponding Author of This Article
Anil Mishra, PhD, Endowed Chair and Professor of Medicine, Department of Medicine, Section of Pulmonary Diseases, Tulane Eosinophilic Disorders Center, Tulane University School of Medicine, SL-9, 1430, Tulane Avnue, New Orleans, LA 70112, United States. amishra@tulane.edu
Research Domain of This Article
Gastroenterology & Hepatology
Article-Type of This Article
Review
Open-Access Policy of This Article
This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
Murli Manohar, Alok Kumar Verma, Sathisha Upparahalli Venkateshaiah, Nathan L Sanders, Anil Mishra, Department of Medicine, Section of Pulmonary Diseases, Tulane Eosinophilic Disorders Center, Tulane University School of Medicine, New Orleans, LA 70112, United States
Author contributions: Manohar M drafted the manuscript and prepared all figures; Verma AK, Venkateshaiah SU and Sanders NL contributed and critically reviewed the manuscript; Mishra A designed, conceived and provided financial assistance.
Supported by National Institutes of Health, Nos. R01 DK067255 and R01 AI080581.
Conflict-of-interest statement: All authors declare no conflict of interests for this review.
Open-Access: This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
Correspondence to: Anil Mishra, PhD, Endowed Chair and Professor of Medicine, Department of Medicine, Section of Pulmonary Diseases, Tulane Eosinophilic Disorders Center, Tulane University School of Medicine, SL-9, 1430, Tulane Avnue, New Orleans, LA 70112, United States. amishra@tulane.edu
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Received: June 8, 2016 Peer-review started: June 13, 2016 First decision: July 20, 2016 Revised: July 23, 2016 Accepted: August 15, 2016 Article in press: August 16, 2016 Published online: February 6, 2017 Processing time: 226 Days and 12.5 Hours
Core Tip
Core tip: Pancreatitis is an acute or chronic inflammatory disease of the pancreas and characterized by destruction of acinar cells, which lead activation of several inflammatory cells like macrophages and granulocytes which secrete number of pro-inflammatory cytokines. These pro-inflammatory cytokines activate pancreatic stellate cells, i.e., the key cells of pancreatic fibrosis. Various molecular signaling pathways (i.e., transforming growth factor-β/SMAD, mitogen-activated protein kinases, Rho kinase, Janus kinase/signal transducers and activators, and phosphatidylinositol 3 kinase) are known to have critical role in the activation of pancreatic stellate cells in chronic pancreatitis and development of pancreatic fibrosis that lead to the pancreatic carcinoma.
