Xie ZX, Li Y, Yang AM, Wu D, Wang Q. Pathogenesis of chronic enteropathy associated with the SLCO2A1 gene: Hypotheses and conundrums. World J Gastroenterol 2024; 30(19): 2505-2511 [PMID: 38817656 DOI: 10.3748/wjg.v30.i19.2505]
Corresponding Author of This Article
Qiang Wang, MD, Assistant Professor, Department of Gastroenterology, Peking Union Medical College Hospital, No. 1 Shuaifuyuan, Dongcheng District, Beijing 100730, China. pekingunion@aliyun.com
Research Domain of This Article
Pathology
Article-Type of This Article
Minireviews
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/
World J Gastroenterol. May 21, 2024; 30(19): 2505-2511 Published online May 21, 2024. doi: 10.3748/wjg.v30.i19.2505
Pathogenesis of chronic enteropathy associated with the SLCO2A1 gene: Hypotheses and conundrums
Zhi-Xin Xie, Yue Li, Ai-Ming Yang, Dong Wu, Qiang Wang
Zhi-Xin Xie, Yue Li, Ai-Ming Yang, Dong Wu, Qiang Wang, State Key Laboratory of Complex Severe and Rare Diseases, Department of Gastroenterology, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences, Beijing 100730, China
Zhi-Xin Xie, Department of Clinical Medicine, Peking Union Medical College, Chinese Academy of Medical Sciences, Beijing 100730, China
Author contributions: Xie ZX drafted the article; Li Y, Yang AM, Wu D, and Wang Q made critical revisions related to important intellectual content of the manuscript and made final approval of the version of the article to be published.
Supported bythe National High-Level Hospital Clinical Research Fund, No. 2022-PUMCH-A-020; and the Undergraduate Teaching Reform and Innovation Project, No. 2022zlgc0108.
Conflict-of-interest statement: All the authors report no relevant conflicts of interest for this article.
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: https://creativecommons.org/Licenses/by-nc/4.0/
Corresponding author: Qiang Wang, MD, Assistant Professor, Department of Gastroenterology, Peking Union Medical College Hospital, No. 1 Shuaifuyuan, Dongcheng District, Beijing 100730, China. pekingunion@aliyun.com
Received: January 14, 2024 Revised: March 18, 2024 Accepted: April 25, 2024 Published online: May 21, 2024 Processing time: 126 Days and 18.1 Hours
Core Tip
Core Tip: Chronic enteropathy associated with SLCO2A1 gene (CEAS) is a complex gastroenterological condition characterized by multiple ulcers in the small intestine with chronic bleeding and protein loss. This review explores potential mechanisms underlying the pathogenesis of CEAS, focusing on the role of SLCO2A1-encoded prostaglandin transporter OATP2A1 and its impact on prostaglandin E2 (PGE2) levels. Studies suggest that elevated PGE2 levels contribute to mucosal damage, inflammation, and disruption of the intestinal barrier. The effects of PGE2 on macrophage activation, Maxi-Cl channel functionality, and its interaction with nonsteroidal anti-inflammatory drugs also play crucial roles in the progression of CEAS. Understanding the delicate balance of its protective and pro-inflammatory effects as well as the complex interactions within the gastrointestinal tract can shed light on potential therapeutic targets for CEAS and guide the development of novel, targeted therapies.
