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肠道纤维化的细胞和分子介质。

Cellular and Molecular Mediators of Intestinal Fibrosis.

机构信息

Centre for Inflammatory Bowel Diseases, Fremantle Hospital, Fremantle, WA, Australia.

University Department of Medicine and Pharmacology, University of Western Australia, Fremantle Hospital, Freemantle, WA, Australia.

出版信息

J Crohns Colitis. 2017 Dec 4;11(12):1491-1503. doi: 10.1016/j.crohns.2014.09.008.

DOI:10.1016/j.crohns.2014.09.008
PMID:25306501
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5885809/
Abstract

Intestinal fibrosis is a major complication of the inflammatory bowel diseases (IBD) and although inflammation is necessary for its development, it would appear that it plays a minor role in its progression as anti-inflammatory treatments in IBD do not prevent fibrosis once it has started. The processes that regulate fibrosis would thus appear to be distinct from those regulating inflammation and, therefore, a detailed understanding of these pathways is vital to the development of anti-fibrogenic strategies. There have been several recent reviews exploring what is known, and what remains unknown, about the development of intestinal fibrosis. This review is designed to add to this literature but with a focus on the cellular components that are involved in the development of fibrogenesis and the major molecular mediators that impact on these cells. The aim is to heighten the understanding of the factors involved in intestinal fibrogenesis so that detailed research can be encouraged in order to advance the processes that could lead to effective treatments.

摘要

肠纤维化是炎症性肠病(IBD)的主要并发症,尽管炎症是其发展所必需的,但似乎在其进展中炎症的作用较小,因为 IBD 的抗炎治疗并不能预防纤维化的发生。因此,调节纤维化的过程似乎与调节炎症的过程不同,因此,对这些途径的详细了解对于开发抗纤维化策略至关重要。最近有几篇综述探讨了关于肠道纤维化发展的已知和未知内容。本综述旨在为这一文献增添内容,但重点是参与纤维化发生的细胞成分以及影响这些细胞的主要分子介质。目的是提高对肠道纤维化发生相关因素的认识,以便鼓励进行详细研究,从而推进可能导致有效治疗的过程。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9bdc/5885809/82e28e4661f6/j.crohns.2014.09.00805.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9bdc/5885809/07ab853853fc/j.crohns.2014.09.00801.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9bdc/5885809/7cd230e58dfe/j.crohns.2014.09.00802.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9bdc/5885809/e99f01a75814/j.crohns.2014.09.00803.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9bdc/5885809/1338687cb87a/j.crohns.2014.09.00804.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9bdc/5885809/82e28e4661f6/j.crohns.2014.09.00805.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9bdc/5885809/07ab853853fc/j.crohns.2014.09.00801.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9bdc/5885809/7cd230e58dfe/j.crohns.2014.09.00802.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9bdc/5885809/e99f01a75814/j.crohns.2014.09.00803.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9bdc/5885809/1338687cb87a/j.crohns.2014.09.00804.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9bdc/5885809/82e28e4661f6/j.crohns.2014.09.00805.jpg

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