New Insights into the Pathogenesis of Intestinal Fibrosis in Inflammatory Bowel Diseases: Focusing on Intestinal Smooth Muscle Cells.

Autor:	Kalafateli M; Department of Gastroenterology, General Hospital of Patras, Patras, Greece., Tourkochristou E; Division of Hematology, Department of Internal Medicine, Medical School, University of Patras, Patras, Greece., Tsounis EP; Division of Hematology, Department of Internal Medicine, Medical School, University of Patras, Patras, Greece., Aggeletopoulou I; Division of Gastroenterology, Department of Internal Medicine, University Hospital of Patras, Patras, Greece., Triantos C; Division of Hematology, Department of Internal Medicine, Medical School, University of Patras, Patras, Greece.
Jazyk:	angličtina
Zdroj:	Inflammatory bowel diseases [Inflamm Bowel Dis] 2024 Dec 16. Date of Electronic Publication: 2024 Dec 16.
DOI:	10.1093/ibd/izae292
Abstrakt:	Strictures in inflammatory bowel disease, especially Crohn's disease (CD), are characterized by increased intestinal wall thickness, which, according to recent accumulating data, is mainly attributed to the expansion of the intestinal smooth muscle layers and to a lesser extent to collagen deposition. In this review, we will discuss the role of intestinal smooth muscle cells (SMCs) as crucial orchestrators of stricture formation. Activated SMCs can synthesize extracellular matrix (ECM), thus contributing to intestinal fibrosis, as well as growth factors and cytokines that can further enhance ECM production, stimulate other surrounding mesenchymal and immune cells, and increase SMC proliferation via paracrine or autocrine signaling. There is also evidence that, in stricturing CD, a phenotypic modulation of SMC toward a myofibroblast-like synthetic phenotype takes place. Moreover, the molecular mechanisms and signaling pathways that regulate SMC hyperplasia/hypertrophy will be extensively reviewed. The understanding of the cellular network and the molecular background behind stricture formation is essential for the design of effective anti-fibrotic strategies, and SMCs might be a promising therapeutic target in the future. (© The Author(s) 2024. Published by Oxford University Press on behalf of Crohn’s & Colitis Foundation. All rights reserved. For commercial re-use, please contact reprints@oup.com for reprints and translation rights for reprints. All other permissions can be obtained through our RightsLink service via the Permissions link on the article page on our site—for further information please contact journals.permissions@oup.com.)
Databáze:	MEDLINE
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