| ISSN |
1007-9327 (print) and 2219-2840 (online) |
| Open Access |
This article is an open-access article that was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution NonCommercial (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/ |
| Copyright |
© The Author(s) 2024. Published by Baishideng Publishing Group Inc. All rights reserved. |
| Article Reprints |
For details, please visit: http://www.wjgnet.com/bpg/gerinfo/247
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| Permissions |
For details, please visit: http://www.wjgnet.com/bpg/gerinfo/207
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| Publisher |
Baishideng Publishing Group Inc, 7041 Koll Center Parkway, Suite 160, Pleasanton, CA 94566, USA |
| Website |
http://www.wjgnet.com |
| Category |
Gastroenterology & Hepatology |
| Manuscript Type |
Review |
| Article Title |
Trypsin in pancreatitis: The culprit, a mediator, or epiphenomenon?
|
| Manuscript Source |
Unsolicited Manuscript |
| All Author List |
Anna S Gukovskaya, Markus M Lerch, Julia Mayerle, Matthias Sendler, Bao-An Ji, Ashok K Saluja, Fred S Gorelick and Ilya Gukovsky |
| ORCID |
|
| Funding Agency and Grant Number |
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| Corresponding Author |
Anna S Gukovskaya, AGAF, DSc, PhD, Director, Director, Full Professor, Senior Scientist, Department of Medicine, David Geffen School of Medicine, University of California at Los Angeles, 11301 Wilshire Blvd, Bldg. 258/340, Los Angeles, CA 90073, United States. agukovsk@ucla.edu |
| Key Words |
Pancreatic acinar cell; Hereditary pancreatitis; Autophagy; Endolysosomal system; Cholecystokinin; Cerulein; Cathepsin |
| Core Tip |
Pancreatitis is a common life-threatening disease of the exocrine pancreas. Its pathogenesis remains obscure, and no specific/effective treatments are available. The current paradigm is that pancreatitis is initiated by premature, intra-acinar-cell conversion of trypsinogen to trypsin. This 130-year-old concept has only recently been tested in genetic mouse models. Our review analyzes the mechanisms mediating trypsinogen activation and protecting against its’ effects, controversies in the available data, potential therapeutic approaches, and future research directions. We conclude that intra-acinar trypsinogen activation is not the culprit but at best one of disease mediators, and possibly an epiphenomenon. This conclusion represents a paradigm shift. |
| Publish Date |
2024-10-23 04:32 |
| Citation |
<p>Gukovskaya AS, Lerch MM, Mayerle J, Sendler M, Ji BA, Saluja AK, Gorelick FS, Gukovsky I. Trypsin in pancreatitis: The culprit, a mediator, or epiphenomenon? <i>World J Gastroenterol</i> 2024; 30(41): 4417-4438</p> |
| URL |
https://www.wjgnet.com/1007-9327/full/v30/i41/4417.htm |
| DOI |
https://dx.doi.org/10.3748/wjg.v30.i41.4417 |
