ArticleScientific reports2016
Bcl2 is a critical regulator of bile acid homeostasis by dictating Shp and lncRNA H19 function.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 69 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
69 citing papers in PubMed, 105 citations in OpenAlex.
- LncRNA H19 as a key regulator in biliary atresia: insights into pathogenesis and potential therapeutic targets.Annals of medicine · 2026Review
- MiRNA-29b accelerates the PDGF in exosomes and stimulates hepatic stellate cells to promote liver fibrosis in biliary atresia.European journal of medical research · 2025Article
- LncRNA H19 promoted alcohol-associated liver disease through dysregulation of alternative splicing and methionine metabolism.Hepatology (Baltimore, Md.) · 2025Article
- Therapeutic Potential of Cranberry Proanthocyanidins in Addressing the Pathophysiology of Metabolic Syndrome: A Scrutiny of Select Mechanisms of Action.Antioxidants (Basel, Switzerland) · 2025Article
- Dynamic role of exosomal long non-coding RNA in liver diseases: pathogenesis and diagnostic aspects.Hepatology international · 2024Review
- Diverse functions of SOX9 in liver development and homeostasis and hepatobiliary diseases.Genes & diseases · 2024Review
- HSDL2 links nutritional cues to bile acid and cholesterol homeostasis.Science advances · 2024Article
- Glycomacropeptide as an Efficient Agent to Fight Pathophysiological Mechanisms of Metabolic Syndrome.Nutrients · 2024Article
- Hepatocyte miR-21-5p-deficiency alleviates APAP-induced liver injury by inducing PPARγ and autophagy.Toxicological sciences : an official journal of the Society of Toxicology · 2024Article
- Recent insights into the pathogenesis and therapeutic targets of chronic liver diseases.eGastroenterology · 2023Article
- M1 macrophage-derived exosomes promote autoimmune liver injury by transferring long noncoding RNA H19 to hepatocytes.MedComm · 2023Article
- Review
- High expression of centromere protein N as novel biomarkers for gastric adenocarcinoma.Cancer reports (Hoboken, N.J.) · 2023Article
- Bile acids and their receptors: modulators and therapeutic targets in liver inflammation.Seminars in immunopathology · 2022Review
- MiR-200c-3p targets SESN1 and represses the IL-6/AKT loop to prevent cholangiocyte activation and cholestatic liver fibrosis.Laboratory investigation; a journal of technical methods and pathology · 2022Article
- The Role of Epigenetics in Primary Biliary Cholangitis.International journal of molecular sciences · 2022Review
- Long Noncoding RNAs and Human Liver Disease.Annual review of pathology · 2022Review
- Long Noncoding RNA H19: A Key Player in Liver Diseases.Hepatology (Baltimore, Md.) · 2021Review
- Noncoding RNAs as Promising Diagnostic Biomarkers and Therapeutic Targets in Intestinal Fibrosis of Crohn's Disease: The Path From Bench to Bedside.Inflammatory bowel diseases · 2021Review
- The long and the small collide: LncRNAs and small heterodimer partner (SHP) in liver disease.Molecular and cellular endocrinology · 2021Review
9 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
10 authors at 7 institutions in 3 countries.
Funding
Abstract
Bile acid (BA) metabolism is tightly controlled by nuclear receptor signaling to coordinate regulation of BA synthetic enzymes and transporters. Here we reveal a molecular cascade consisting of the antiapoptotic protein BCL2, nuclear receptor Shp, and long non-coding RNA (lncRNA) H19 to maintain BA homeostasis. Bcl2 was overexpressed in liver of C57BL/6J mice using adenovirus mediated gene delivery for two weeks. Hepatic overexpression of Bcl2 caused drastic accumulation of serum BA and bilirubin levels and dysregulated BA synthetic enzymes and transporters. Bcl2 reactivation triggered severe liver injury, fibrosis and inflammation, which were accompanied by a significant induction of H19. Bcl2 induced rapid SHP protein degradation via the activation of caspase-8 pathway. The induction of H19 in Bcl2 overexpressed mice was contributed by a direct loss of Shp transcriptional repression. H19 knockdown or Shp re-expression largely rescued Bcl2-induced liver injury. Strikingly different than Shp, the expression of Bcl2 and H19 was hardly detectable in adult liver but was markedly increased in fibrotic/cirrhotic human and mouse liver. We demonstrated for the first time a detrimental effect of Bcl2 and H19 associated with cholestatic liver fibrosis and an indispensable role of Shp to maintain normal liver function.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.