ArticleScientific reports2024
GGT1 is a SNP eQTL gene involved in STAT3 activation and associated with the development of Post-ERCP pancreatitis.
Article in Scientific reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- Article
- Cracking the code of post-ERCP pancreatitis: predictors, prevention, and proven strategies from 3323 surgeon-led procedures.Surgical endoscopy · 2026Article
- Gamma-glutamyl transferase as a redox-gatekeeper biomarker for pancreatic cystic neoplasms: A concise roadmap from epidemiology to bedside.World journal of gastroenterology · 2026Article
- STATs Signaling Pathways in Acute Pancreatitis: Mechanisms and Regulation.International journal of medical sciences · 2026Review
- Clinical and stool microbiome correlates of simple post-ERCP hyperamylasemia in children undergoing therapeutic ERCP for pancreatobiliary obstructive disorders: an exploratory pilot study.Frontiers in pediatrics · 2026Article
- Post-endoscopic retrograde cholangiopancreatography pancreatitis: Mechanistic pathways, diagnostic benchmarks, and emerging and mitochondria-targeted therapies.World journal of gastrointestinal surgery · 2025Review
- Post Endoscopic Retrograde Cholangiopancreatography Pancreatitis: Novel Mechanisms and Prevention by Drugs.United European gastroenterology journal · 2025Review
- LRG1 inhibition promotes acute pancreatitis recovery by inducing cholecystokinin Type 1 receptor expression via Akt.Theranostics · 2025Article
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Authors and funding
19 authors.
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Abstract
Post-ERCP pancreatitis (PEP) is an acute pancreatitis caused by endoscopic-retrograde-cholangiopancreatography (ERCP). About 10% of patients develop PEP after ERCP. Here we show that gamma-glutamyltransferase 1 (GGT1)-SNP rs5751901 is an eQTL in pancreatic cells associated with PEP and a positive regulator of the IL-6 amplifier. More PEP patients had the GGT1 SNP rs5751901 risk allele (C) than that of non-PEP patients at Hokkaido University Hospital. Additionally, GGT1 expression and IL-6 amplifier activation were increased in PEP pancreas samples with the risk allele. A mechanistic analysis showed that IL-6-mediated STAT3 nuclear translocation and STAT3 phosphorylation were suppressed in GGT1-deficient cells. Furthermore, GGT1 directly associated with gp130, the signal-transducer of IL-6. Importantly, GGT1-deficiency suppressed inflammation development in a STAT3/NF-κB-dependent disease model. Thus, the risk allele of GGT1-SNP rs5751901 is involved in the pathogenesis of PEP via IL-6 amplifier activation. Therefore, the GGT1-STAT3 axis in pancreas may be a prognosis marker and therapeutic target for PEP.
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