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. 2024 Dec 3;13(23):1997. doi: 10.3390/cells13231997

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© 2024 by the authors.

Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/).

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The pathogenetic and fibrotic mechanisms of BA. The etiology of BA may involve complex interactions among multiple factors, including viral infections, toxins, and genetic elements. Following BA, there is bile duct proliferation, disruption of cell junctions, altered cell polarity, and activation of the immune response. These changes lead to HSC activation, excessive ECM accumulation, and autoimmunity, ultimately resulting in liver fibrosis, cirrhosis, and liver failure, necessitating liver transplantation to extend the patient’s lifespan. BA: biliary atresia; HSCs: hepatic stellate cells; ECM: extracellular matrix. Diagrams were created with the help of BioRender software (© 2024 BioRender).