ArticleOncotarget2016
Chenodeoxycholic acid activates NLRP3 inflammasome and contributes to cholestatic liver fibrosis.
Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 80 papers, 1 of them a synthesis that pooled it.
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Who cites it
80 citing papers in PubMed, 1 synthesis or guideline pooled it, 138 citations in OpenAlex.
- Gut microbiome and atrial fibrillation: mechanistic insights metabolites and comorbidities. Systematic review.Gut microbes · 2025Pooled it
- Microbiota-gut-brain axis and bile acids-driven neuromodulation.Neural regeneration research · 2026Article
- A novel link between enhanced chenodeoxycholic acid synthesis and multi-walled carbon nanotubes-induced proliferation inhibition and apoptosis in human ocular cells.Journal of advanced research · 2026Article
- Bat-Inspired Longevity: Immune Damage Management and Nutritional Modulation for Healthy Aging.International journal of molecular sciences · 2026Review
- Arrb2 in hepatocytes promotes M2 macrophage polarization, ameliorates hepatic ischemia-reperfusion injury through upregulating metabolite 6-ketoLCA.Hepatology communications · 2026Article
- Review
- The NLRP3 inflammasome in metabolic dysfunction-associated steatotic liver disease: role and advances in therapeutic targeting.Frontiers in immunology · 2026Review
- The role of bile acid-activated receptor TGR5 in inflammation and liver diseases.Frontiers in physiology · 2026Review
- The bile acid-gut microbiota-vitamin D axis: new insights into biliary atresia.Frontiers in cellular and infection microbiology · 2026Review
- Hepatoprotective Effect ofFood science & nutrition · 2026Article
- The role of gut microbiota in neuropathic pain: insights into immune mechanisms.The journal of headache and pain · 2025Review
- Impact of gut microbiome on atrial fibrillation: Mechanistic insights and future directions in individualized medicine.World journal of cardiology · 2025Review
- New drug therapies for metabolic dysfunction-associated steatohepatitis.Liver research (Beijing, China) · 2025Review
- Modeling "Two-Hit" Severe Pneumonia in Mice: Pathological Characteristics and Mechanistic Studies.Inflammation · 2025Article
- Emerging role of bile acids in colorectal liver metastasis: From molecular mechanism to clinical significance (Review).International journal of oncology · 2025Review
- Effects of Bile Acids on Growth Performance, Hepatopancreatic Antioxidant Capacity, Intestinal Immune-Related Gene Expression, and Gut Microbiota ofAnimals : an open access journal from MDPI · 2025Article
- Goose Deoxycholic Acid Ameliorates Liver Injury in Laying Hens with Fatty Liver Hemorrhage Syndrome by Inhibiting the Inflammatory Response.International journal of molecular sciences · 2025Article
- Ursodeoxycholic and chenodeoxycholic bile acids alleviate endotoxininduced acute lung injury in rats by modulating aquaporin expression and pathways associated with apoptosis and inflammation.Frontiers in pharmacology · 2025Article
- Bile salt hydrolase: a key player in gut microbiota and its implications for metabolic dysfunction-associated steatotic liver disease.Microbiome research reports · 2025Review
- Ursodeoxycholic and chenodeoxycholic bile acids attenuate systemic and liver inflammation induced by lipopolysaccharide in rats.Molecular and cellular biochemistry · 2025Article
20 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Accumulation of hydrophobic bile acids in the liver contributes to cholestatic liver injury. Inflammation induced by excessive bile acids is believed to play a crucial role, however, the mechanisms of bile acids triggered inflammatory response remain unclear. Recent studies have highlighted the effect of NLRP3 inflammasome in mediating liver inflammation and fibrosis. In this study, we for the first time showed that chenodeoxycholic acid (CDCA), the major hydrophobic primary bile acid involved in cholestatic liver injury, could dose-dependently induce NLRP3 inflammasome activation and secretion of pro-inflammatory cytokine-IL-1β in macrophages by promoting ROS production and K+ efflux. Mechanistically, CDCA triggered ROS formation in part through TGR5/EGFR downstream signaling, including protein kinase B, extracellular regulated protein kinases and c-Jun N-terminal kinase pathways. Meanwhile, CDCA also induced ATP release from macrophages which subsequently causes K+ efflux via P2X7 receptor. Furthermore, in vivo inhibition of NLRP3 inflammasome with caspase-1 inhibitor dramatically decreased mature IL-1β level of liver tissue and ameliorated liver fibrosis in bile duct ligation (BDL) mouse model. In conclusion, excessive CDCA may represent an endogenous danger signal to activate NLRP3 inflammasome and initiate liver inflammation during cholestasis. Our finding offers a mechanistic basis to ameliorate cholestatic liver fibrosis by targeting inflammasome activation.
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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.