ArticleCell reports. Medicine2023
Bile acid metabolomics identifies chenodeoxycholic acid as a therapeutic agent for pancreatic necrosis.
Article in Cell reports. Medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 27 citations in OpenAlex.
- Improved catalytic efficiency of P450 OleP for converting lithocholic acid into murideoxycholic and ursodeoxycholic acids through semi-rational and rational design.Synthetic and systems biotechnology · 2027Article
- Gut microbiota-derived riboflavin mediates protective effects of MUC2 in acute pancreatitis via CD40-macrophage pathway.Microbiome · 2026Article
- Chenodeoxycholic acid redirects the bile acid synthetic pathway to limit pro-inflammatory neutrophil infiltration and alleviate colitis.Molecular therapy : the journal of the American Society of Gene Therapy · 2026Article
- Review
- Odoribacter laneus protects intestinal barrier by bile acid-FXR axis in acute pancreatitis.AMB Express · 2026Article
- Targeted Metabolomics Uncovers NorCA's Role as a Potent Immunomodulator in Acute Pancreatitis by Promoting Macrophage Reprogramming and Efferocytosis.International journal of molecular sciences · 2026Article
- The functions of gut microbiota-mediated bile acid metabolism in intestinal immunity.Journal of advanced research · 2026Review
- Bile acid metabolism dysregulation following Helicobacter pylori eradication promotes plasmid-mediated antimicrobial resistance in the gut microbiome.The ISME journal · 2026Article
- Potential influence of gut microbiota on the process of hypertriglyceridemia-aggravated acute pancreatitis.World journal of gastroenterology · 2026Review
- Blautia coccoides Alleviates Acute Pancreatitis via Bile Salt Hydrolase-mediated Deoxycholic Acid Production and Farnesoid X Receptor Signaling.Cellular and molecular gastroenterology and hepatology · 2026Article
- Modulating Bile Acid Metabolism: The Role of Blautia coccoides in Acute Pancreatitis.Cellular and molecular gastroenterology and hepatology · 2026Article
- TUDCA-3S is Associated with Acute Pancreatitis Severity and Pro-Inflammatory Macrophage Activation Involving S100A8/IL-17 Signaling.Journal of inflammation research · 2026Article
- Association between prediagnostic serum metabolites and pancreatic ductal adenocarcinoma risk in two prospective cohorts.International journal of cancer · 2025Article
- Pharmacological Inhibition of Phosphoglycerate Kinase 1 Reduces OxiDative Stress and Restores Impaired Autophagy in Experimental Acute Pancreatitis.Inflammation · 2025Article
- Dietary emulsifier carboxymethylcellulose-induced gut dysbiosis and SCFA reduction aggravate acute pancreatitis through classical monocyte activation.Microbiome · 2025Article
- Investigation of the mechanism of chenodeoxycholic acid in treating acute lung injury through network pharmacology and experimental validation.Scientific reports · 2025Article
- Profiling bile acid composition in bile from mice of different ages and sexes.Frontiers in physiology · 2025Article
- Inhibition of CD53 Reduces the Formation of ROS-Induced Neutrophil Extracellular Traps and Protects Against Inflammatory Injury in Acute Pancreatitis.Journal of inflammation research · 2025Article
- Conjugated bile acids alleviate acute pancreatitis through inhibition of TGR5 and NLRP3 mediated inflammation.Journal of translational medicine · 2024Article
- Role and mechanism of myonectin in severe acute pancreatitis: a crosstalk between skeletal muscle and pancreas.Skeletal muscle · 2024Article
Corrections and comments
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Authors and funding
14 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Bile acids are altered and associated with prognosis in patients with acute pancreatitis (AP). Here, we conduct targeted metabolomic analyses to detect bile acids changes in patients during the acute (n = 326) and the recovery (n = 133) phases of AP, as well as in healthy controls (n = 60). Chenodeoxycholic acid (CDCA) decreases in the acute phase, increases in the recovery phase, and is associated with pancreatic necrosis. CDCA and its derivative obeticholic acid exhibit a protective effect against acinar cell injury in vitro and pancreatic necrosis in murine models, and RNA sequencing reveals that the oxidative phosphorylation pathway is mainly involved. Moreover, we find that overexpression of farnesoid X receptor (FXR, CDCA receptor) inhibits pancreatic necrosis, and interfering expression of FXR exhibits an opposite phenotype in mice. Our results possibly suggest that targeting CDCA is a potential strategy for the treatment of acinar cell necrosis in AP, but further verification is needed.
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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 Socratic graph.