ArticleClinical and translational gastroenterology2022
Beta-amyloid Deposition in Biliary Atresia Reduces Liver Regeneration by Inhibiting Energy Metabolism and Mammalian Target of Rapamycin Signaling.
Article in Clinical and translational gastroenterology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 8 citations in OpenAlex.
- Amyloid precursor protein as a fibrosis marker in infants with biliary atresia.Pediatric research · 2025Article
- Organoids in biliary atresia.World journal of pediatric surgery · 2025Review
- Organoids in biliary research: insights into developmental signaling and applications in disease modeling.Frontiers in cell and developmental biology · 2025Review
- Interleukin 17A promotes glycolysis to activate human hepatic stellate cells by mediating the TRAF2/TRAF5/HuR/PFKFB3 axis.Central-European journal of immunology · 2024Article
- Does amyloid β precursor protein gene expression have a role in diagnosis of biliary atresia?Clinical and experimental hepatology · 2023Article
- Comparative proteomics analyses of whey proteins from breastmilk collected from two ethnic groups in northeast China.Food chemistry: X · 2023Article
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
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Abstract
introductionBiliary atresia (BA) is a devastating obstructive bile duct disease found in newborns. This study aims to investigate the roles and involved mechanisms of beta-amyloid (Aβ) in the pathogenesis of BA.
methodsWe examined the distribution of Aβ protein and its precursor in the livers of patients with BA. A murine liver organoid and a zebrafish model were established to investigate the exact roles of Aβ in liver regeneration for BA.
resultsBoth Aβ mRNA and protein significantly increased in livers of infants with BA and deposited around the central vein. In the plasma, Aβ elevated significantly in patients with BA and positively correlated with liver injury progression. In vitro , Aβ treatment induced abnormal morphology and caused impaired growth in liver organoids. Energy metabolism analysis demonstrated Aβ increased aerobic glycolysis and reduced ATP synthase in organoids, in which the mammalian target of rapamycin signaling was suppressed. In vivo , Aβ42 exposure caused liver degeneration in zebrafish larvae. DISCUSSION: Aβ depositing in livers of infants with BA reduced the liver regeneration through attenuating mitochondrial respiration and mammalian target of rapamycin signaling.
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