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与基因相关的慢性肠病的发病机制:假说与困惑。

Pathogenesis of chronic enteropathy associated with the gene: Hypotheses and conundrums.

机构信息

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.

Department of Clinical Medicine, Peking Union Medical College, Chinese Academy of Medical Sciences, Beijing 100730, China.

出版信息

World J Gastroenterol. 2024 May 21;30(19):2505-2511. doi: 10.3748/wjg.v30.i19.2505.

Abstract

Chronic enteropathy associated with the gene (CEAS) is a complex gastroenterological condition characterized by multiple ulcers in the small intestine with chronic bleeding and protein loss. This review explores the potential mechanisms underlying the pathogenesis of CEAS, focusing on the role of -encoded prostaglandin transporter OATP2A1 and its impact on prostaglandin E2 (PGE2) levels. Studies have suggested that elevated PGE2 levels contribute to mucosal damage, inflammation, and disruption of the intestinal barrier. The effects of PGE2 on macrophage activation and Maxi-Cl channel functionality, as well as its interaction with nonsteroidal anti-inflammatory drugs play crucial roles in the progression of CEAS. Understanding the balance between its protective and pro-inflammatory effects and the complex interactions within the gastrointestinal tract can shed light on potential therapeutic targets for CEAS and guide the development of novel, targeted therapies.

摘要

与基因(CEAS)相关的慢性肠病是一种复杂的胃肠疾病,其特征是小肠多发性溃疡,伴有慢性出血和蛋白丢失。本综述探讨了 CEAS 发病机制的潜在机制,重点关注了 -编码的前列腺素转运体 OATP2A1 及其对前列腺素 E2(PGE2)水平的影响。研究表明,升高的 PGE2 水平会导致黏膜损伤、炎症和肠道屏障破坏。PGE2 对巨噬细胞激活和 Maxi-Cl 通道功能的影响,以及其与非甾体抗炎药的相互作用,在 CEAS 的进展中起着关键作用。了解其保护和促炎作用之间的平衡以及胃肠道内的复杂相互作用,可以为 CEAS 提供潜在的治疗靶点,并指导新型靶向治疗的发展。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f6e3/11135407/2be83299c645/WJG-30-2505-g001.jpg

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