ArticleCell death & disease2021
Sulfiredoxin-1 attenuates injury and inflammation in acute pancreatitis through the ROS/ER stress/Cathepsin B axis.
Article in Cell death & disease, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers, 1 of them a synthesis that pooled it.
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Who cites it
42 citing papers in PubMed, 1 synthesis or guideline pooled it, 65 citations in OpenAlex.
- Reactive oxygen species and oxidative stress in acute pancreatitis: Pathogenesis and new therapeutic interventions.World journal of gastroenterology · 2024Pooled it
- Fibulin-1 Improves Caerulein-Induced Acute Pancreatitis In Vitro by Inhibiting Ferroptosis.Journal of biochemical and molecular toxicology · 2026Article
- PVNJournal of neuroinflammation · 2026Article
- Repeated photobiological regulation therapy alleviates inflammation in mice with experimental acute pancreatitis through ROS/NF-κB pathway.Lasers in medical science · 2026Article
- Article
- Integrative Genomics Reveals Causal Pleiotropy and Therapeutic Opportunities at the Interface of Acute Pancreatitis and Infection.Journal of hepato-biliary-pancreatic sciences · 2026Article
- Acute pancreatitis: mechanisms and therapeutic approaches.Signal transduction and targeted therapy · 2026Review
- Blockade of calcium-activated chloride channel ANO1 ameliorates ionizing radiation-induced intestinal injury.Journal of advanced research · 2026Article
- Mechanistic insights into how intrapancreatic fat deposition drives the development of acute pancreatitis.International journal of biological sciences · 2026Review
- Glucose-to-albumin ratio and mortality in ICU patients with acute pancreatitis.Open medicine (Warsaw, Poland) · 2026Article
- EP300 confers protection against acute pancreatitis via acetylating HSF1 and promoting PRKN-mediated mitophagy in pancreatic acinar cells.Cell communication and signaling : CCS · 2025Article
- Roles of chemokines in pancreatitis: A review.World journal of gastrointestinal pathophysiology · 2025Review
- Targeting Cathepsins in Neurodegeneration: Biochemical Advances.Biomedicines · 2025Review
- Clock genes in pancreatic disease progression: from circadian regulation to dysfunction.Annals of medicine · 2025Review
- UCP2 Upregulates ACSL3 to Enhance Lipid Droplet Release from Acinar Cells and Modulates the Sirt1/Smad3 Pathway to Promote Macrophage-to-Myofibroblast Transition in Chronic Pancreatitis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Ubiquitin-specific protease 7 regulates macrophage polarization via pyruvate kinase M2-mediated metabolic reprogramming in severe acute pancreatitis.Cell death & disease · 2025Article
- Redox regulation by sulfiredoxin-1: bridging cysteine oxidation and liver disease therapeutics.Experimental & molecular medicine · 2025Review
- Inhibition of PRC1 elicits immunogenic cell death by triggering ROS-dependent ER stress in colorectal cancer via the Wnt/β-catenin signaling pathway.Biology direct · 2025Article
- Adipocyte CLDN5 promotes thermogenesis and energy expenditure through regulation of IL10 expression.Nature communications · 2025Article
- The desulfinylation enzyme sulfiredoxin-1 attenuates HSC activation and liver fibrosis by modulating the PTPN12-NLRP3 axis.Hepatology (Baltimore, Md.) · 2025Article
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 1 country.
Funding
Abstract
Acinar cell injury and the inflammatory response are critical bioprocesses of acute pancreatitis (AP). We investigated the role and underlying mechanism of sulfiredoxin-1 (Srxn1) in AP. Mild AP was induced by intraperitoneal injection of cerulein and severe AP was induced by partial duct ligation with cerulein stimulation or intraperitoneal injection of L-arginine in mice. Acinar cells, neutrophils, and macrophages were isolated. The pancreas was analyzed by histology, immunochemistry staining, and TUNEL assays, and the expression of certain proteins and RNAs, cytokine levels, trypsin activity, and reactive oxygen species (ROS) levels were determined. Srxn1 was inhibited by J14 or silenced by siRNA, and overexpression was introduced by a lentiviral vector. Transcriptomic analysis was used to explore the mechanism of Srxn1-mediated effects. We also evaluated the effect of adeno-associated virus (AAV)-mediated overexpression of Srxn1 by intraductal administration and the protection of AP. We found that Srxn1 expression was upregulated in mild AP but decreased in severe AP. Inhibition of Srxn1 increased ROS, histological score, the release of trypsin, and inflammatory responses in mice. Inhibition of Srxn1 expression promoted the production of ROS and induced apoptosis, while overexpression of Srxn1 led to the opposite results in acinar cells. Furthermore, inhibition of Srxn1 expression promoted the inflammatory response by accumulating and activating M1 phenotype macrophages and neutrophils in AP. Mechanistically, ROS-induced ER stress and activation of Cathepsin B, which converts trypsinogen to trypsin, were responsible for the Srxn1 inhibition-mediated effects on AP. Importantly, we demonstrated that AAV-mediated overexpression of Srxn1 attenuated AP in mice. Taken together, these results showed that Srxn1 is a protective target for AP by attenuating acinar injury and inflammation through the ROS/ER stress/Cathepsin B axis.
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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.