Biliary fibrosis is an important but neglected pathological feature in hepatobiliary disorders: from molecular mechanisms to clinical implications.
Details
Serval ID
serval:BIB_04AC9A556203
Type
Article: article from journal or magazin.
Collection
Publications
Institution
Title
Biliary fibrosis is an important but neglected pathological feature in hepatobiliary disorders: from molecular mechanisms to clinical implications.
Journal
Medical review
ISSN
2749-9642 (Electronic)
ISSN-L
2749-9642
Publication state
Published
Issued date
08/2024
Peer-reviewed
Oui
Volume
4
Number
4
Pages
326-365
Language
english
Notes
Publication types: Journal Article ; Review
Publication Status: epublish
Publication Status: epublish
Abstract
Fibrosis resulting from pathological repair secondary to recurrent or persistent tissue damage often leads to organ failure and mortality. Biliary fibrosis is a crucial but easily neglected pathological feature in hepatobiliary disorders, which may promote the development and progression of benign and malignant biliary diseases through pathological healing mechanisms secondary to biliary tract injuries. Elucidating the etiology and pathogenesis of biliary fibrosis is beneficial to the prevention and treatment of biliary diseases. In this review, we emphasized the importance of biliary fibrosis in cholangiopathies and summarized the clinical manifestations, epidemiology, and aberrant cellular composition involving the biliary ductules, cholangiocytes, immune system, fibroblasts, and the microbiome. We also focused on pivotal signaling pathways and offered insights into ongoing clinical trials and proposing a strategic approach for managing biliary fibrosis-related cholangiopathies. This review will offer a comprehensive perspective on biliary fibrosis and provide an important reference for future mechanism research and innovative therapy to prevent or reverse fibrosis.
Keywords
biliary fibrosis, cholangiopathy, etiology, mechanism, therapeutic strategy
Pubmed
Open Access
Yes
Create date
19/08/2024 7:47
Last modification date
20/08/2024 6:23