A narrative review of genes associated with liver fibrosis in biliary atresia.

Autor:	Liu F; Division of Paediatric Surgery, Department of Surgery, School of Clinical Medicine, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Hong Kong, China., Tang CSM; Division of Paediatric Surgery, Department of Surgery, School of Clinical Medicine, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Hong Kong, China., Chung PHY; Division of Paediatric Surgery, Department of Surgery, School of Clinical Medicine, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Hong Kong, China.
Jazyk:	angličtina
Zdroj:	Translational pediatrics [Transl Pediatr] 2024 Aug 31; Vol. 13 (8), pp. 1469-1478. Date of Electronic Publication: 2024 Aug 28.
DOI:	10.21037/tp-24-94
Abstrakt:	Background and Objective: Biliary atresia (BA) is characterized by biliary inflammation and obstruction. In the later phase, liver fibrosis occurs. Although the etiology of BA is believed to be multi-factorial, genetic predisposition has been proposed to play a critical role in the pathogenesis. This review aimed to provide an updated summary of the genes that have been reported to be involved in BA-associated liver fibrosis. Methods: The review was conducted via evaluation of MalaCards (BA disease: MalaCards-research articles, drugs, genes, clinical trials) which is a universally applied website including various human disease database. The database of genes that are involved in liver fibrosis were studied. Key Content and Findings: Thirty-one genes that are associated with BA according to the disease relevance score were reviewed after further evaluations. Eleven genes ( GPT, NR1H4, TGF-B1, MMP7, CCN2, TIMP1, SPP1, ADD3, KRT7, ADD3-AS1, SOX9 ) that are specific and with a potential association with liver fibrosis were selected for detailed description. Increased expression of GPT , TGF-B1 , MMP7 , CCN2 , TIMP1 , SPP1 , ADD3 , KRT7 and ADD3-AS1 maybe associated with the development of liver fibrosis in BA patients, while the expression of NR1H4 and SOX9 are more likely to suppress liver fibrosis. Conclusions: Current scientific evidence using gene database has revealed a close association between genetic anomalies and the pathogenesis of liver fibrosis in BA. With a better understanding of these anomalies, therapy targeting these related genes may be a new therapeutic approach to alleviate liver fibrosis in BA. Competing Interests: Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at https://tp.amegroups.com/article/view/10.21037/tp-24-94/coif). P.H.Y.C. serves as an unpaid editorial board member of Translational Pediatrics from August 2022 to July 2024. The other authors have no conflicts of interest to declare. (2024 Translational Pediatrics. All rights reserved.)
Databáze:	MEDLINE
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