ReviewPancreas2012
Sterile inflammatory response in acute pancreatitis.
Review in Pancreas, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 79 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
79 citing papers in PubMed, 143 citations in OpenAlex.
- Acute pancreatitis: mechanisms and therapeutic approaches.Signal transduction and targeted therapy · 2026Review
- Neutrophil extracellular traps prime the ZBP1-cGAS sensor complex, triggering necroptosis and inflammatory injury in acute pancreatitis.International journal of biological sciences · 2026Article
- IL-1 family of cytokines in gastrointestinal and liver disorders.Nature reviews. Gastroenterology & hepatology · 2026Review
- Integrative single-cell and bulk transcriptomic analysis identify R-loop-associated gene signatures driving immune-inflammatory networks in acute pancreatitis.Frontiers in immunology · 2026Article
- Annexin A1 mRNA-loaded liposomes alleviate acute pancreatitis by suppressing STING pathway and promoting efferocytosis in macrophages.Nature nanotechnology · 2025Article
- Hydrogel Innovations in Biosensing: A New Frontier for Pancreatitis Diagnostics.Bioengineering (Basel, Switzerland) · 2025Review
- LRG1 inhibition promotes acute pancreatitis recovery by inducing cholecystokinin Type 1 receptor expression via Akt.Theranostics · 2025Article
- Case Report: A rare cause of pancreatitis - fish bone.Frontiers in medicine · 2025Article
- Clinical Significance of Low-Density Granulocytes in Acute Pancreatitis.Mediators of inflammation · 2025Article
- Anti-DAMP therapies for acute inflammation.Frontiers in immunology · 2025Review
- Unpacking the sepsis controversy.Trauma surgery & acute care open · 2025Review
- Gut microbiota analysis and LC-MS-based metabolomics to investigate AMPK/NF-κB regulated by Clostridium butyricum in the treatment of acute pancreatitis.Journal of translational medicine · 2024Article
- The TRIM28/miR133a/CD47 axis acts as a potential therapeutic target in pancreatic necrosis by impairing efferocytosis.Molecular therapy : the journal of the American Society of Gene Therapy · 2024Article
- From pancreas to lungs: The role of immune cells in severe acute pancreatitis and acute lung injury.Immunity, inflammation and disease · 2024Review
- Safety and efficacy of early versus late removal of LAMS for pancreatic fluid collections.Endoscopy international open · 2024Article
- Damage-Associated Molecular Patterns, a Class of Potential Psoriasis Drug Targets.International journal of molecular sciences · 2024Review
- Editorial: Immune dysfunction in acute pancreatitis: from bench to bedside research.Frontiers in immunology · 2024Article
- Repetitive Cerulein-Induced Chronic Pancreatitis in Growing Pigs-A Pilot Study.International journal of molecular sciences · 2023Article
- Association analysis between the TLR9 gene polymorphism rs352140 and type 1 diabetes.Frontiers in endocrinology · 2023Article
- New challenges for microRNAs in acute pancreatitis: progress and treatment.Journal of translational medicine · 2022Review
19 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
4 authors at 1 institution in 1 country.
Funding
Abstract
The initial injury in acute pancreatitis is characteristically sterile and results in acinar cells necrosis. Intracellular contents released from damaged cells into the extracellular space serve as damage-associated molecular patterns (DAMPs) that trigger inflammation. There is increasing evidence that this sterile inflammatory response mediated through DAMPs released from necrotic acinar cells is a key determinant of further pancreatic injury, remote organ injury, and disease resolution in experimental models. A number of DAMPS, including high-mobility group box protein 1, DNA, adenosine triphosphate and heat shock protein 70, have been shown to have a role in experimental pancreatitis. Many of these DAMPs are also detectable in the human pancreatitis. Genetic deletion and pharmacologic antagonism demonstrate that specific DAMP receptors, including Toll-like receptor (TLR) 4, TLR9, and P2X7, are also required for inflammation in experimental acute pancreatitis. Downstream DAMP-sensing components include nod-like receptor protein 3, caspase 1, interleukin-1β (IL-1), IL-18, and IL-1 receptor, and also are required for full experimental pancreatitis. These DAMP-mediated pathways provide novel therapeutic targets using antagonists of TLRs and other receptors.
Indexed as
Identifiers
What OpenQuestion holds
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.