Definition and research guide
This page combines a MeSH definition, publication statistics and selected research abstracts. It is a starting point for reading the literature, not a medical textbook or a systematic evidence review.
Content available: 3 complete abstracts (675 words), 9 references. Full article text is not stored or reproduced here; follow the PMID, DOI or PMC links to read the original sources and their access terms.
Definition
Inflammation of the pancreas. Pancreatitis is classified as acute unless there are computed tomographic or endoscopic retrograde cholangiopancreatographic findings of chronic pancreatitis (International Symposium on Acute Pancreatitis, Atlanta, 1992). The two most common forms of acute pancreatitis are alcoholic pancreatitis and gallstone pancreatitis.
Definition: NLM Medical Subject Headings (MeSH) scope note (Public domain (U.S. National Library of Medicine); attribution requested). View the MeSH record.
Also known as: Pancreatitis, Acute; Acute Pancreatitis; Acute Pancreatitides; Pancreatitides, Acute; Pancreatitis, Acute Edematous; Acute Edematous Pancreatitides; Edematous Pancreatitides, Acute; Edematous Pancreatitis, Acute.
Where it fits in the MeSH classification
- Broader topics
- Pancreatic Diseases
- Narrower topics
- Pancreatitis, Acute Hemorrhagic; Pancreatitis, Acute Necrotizing; Pancreatitis, Alcoholic; Pancreatitis, Chronic; Pancreatitis, Graft
Related concepts
- Inflammation
- Pancreas
- Chronic Pancreatitis
- Alcoholic Pancreatitis
Research landscape
PubMed indexes 60,969 records tagged with the MeSH heading “Pancreatitis” (counts retrieved 2026-11-04). 9,659 of them (15.8%) were published from 2020 onward, and the busiest period so far is through 1999 with 27,056 records.
Reviews account for 8,212 records (13.5%) and meta-analyses for 788. Randomized controlled trials number 1,087 (1.8%) as a share of all records on the topic. Randomized trials make up only a small share of this literature, so much of what is known comes from laboratory, observational or descriptive work.
Show the data
| Period | Records |
|---|---|
| through 1999 | 27,056 |
| 2000-2009 | 11,035 |
| 2010-2019 | 13,219 |
| 2020 onward | 9,659 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 8,212 | 13.5% |
| Meta-analyses | 788 | 1.3% |
| Randomized controlled trials | 1,087 | 1.8% |
Method: PubMed query "Pancreatitis"[MeSH Terms] with publication-type and date filters, retrieved 2026-11-04.
Reading the evidence in digestive system and liver
Gut and liver research ranges from laboratory studies of the microbiome to large trials of drugs and surgery. Symptoms such as pain, reflux or bowel change are reported by patients and overlap between conditions, and diet and microbiome studies are mostly observational. Check whether the study measured symptoms, tissue findings or long-term outcomes, how the diagnosis was made and how long people were followed. Nothing here replaces advice from a qualified clinician.
Evidence from open-access studies
These open-access studies come from PubMed’s best-match results for this heading (papers whose main topic it is), ranked here by citation count, with one recent addition. Each abstract is reproduced in full under its recorded open licence so that you can read the authors’ own words. They illustrate the literature; they are not a systematic summary of it. Citation counts measure attention, not reliability or clinical benefit.
| Study / authors | Year | Source label / design | Europe PMC citations | Licence / source |
|---|---|---|---|---|
| Milk fat globule-EGF factor 8/ATP-binding cassette subfamily E member 1 axis maintains mitophagy flux homeostasis to suppress ferroptosis in acute pancreatitis | 2026 | Research article Design not recorded in structured metadata | 3 | cc by PMID 41705299 · DOI · PMC12914346 |
| Targeting mitochondrial phosphatase PGAM5 alleviates ferroptosis and acute pancreatitis by upregulating NRF2-mediated FSP1 expression | 2026 | Research article Design not recorded in structured metadata | 2 | cc by PMID 41723122 · DOI · PMC12966488 |
| Neutrophil extracellular traps prime the ZBP1-cGAS sensor complex, triggering necroptosis and inflammatory injury in acute pancreatitis | 2026 | Research article Design not recorded in structured metadata | 2 | cc by PMID 41800237 · DOI · PMC12965145 |
Milk fat globule-EGF factor 8/ATP-binding cassette subfamily E member 1 axis maintains mitophagy flux homeostasis to suppress ferroptosis in acute pancreatitis [1]
Abstract reading summary — source excerpts
- Opening excerpt
- BackgroundAcute pancreatitis (AP) is a severe inflammatory disorder in which mitochondrial dysfunction and ferroptosis critically drive acinar cell injury.
- Closing excerpt
- This axis suppresses ferroptosis by reducing Fe2+ accumulation and lipid peroxidation, alleviating AP-related pancreatic injury.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (331 words)
BackgroundAcute pancreatitis (AP) is a severe inflammatory disorder in which mitochondrial dysfunction and ferroptosis critically drive acinar cell injury. Our previous work suggested a protective role for exogenous milk fat globule-epidermal growth factor 8 (MFG-E8) in AP. This study aimed to elucidate the molecular mechanism by which endogenous MFG-E8 mitigates mitochondrial damage and ferroptosis during AP.MethodsTwo mouse models of AP were used for in vivo studies, while cerulein + lipopolysaccharide-induced mitophagy and ferroptosis in AR42J cells (cells of the rat exocrine pancreas) for in vitro studies. Mfge8 gene-defective mice and lentivirus were utilised to downregulate MFG-E8 expression in mice and overexpress MFG-E8 in cells, respectively. Dual gene modification was employed to overexpress MFG-E8 and simultaneously knockdown adenosine triphosphate (ATP)-binding cassette subfamily E member 1 (ABCE1) in vitro. One mitophagy agonist and two ferroptosis inhibitors were used in both in vitro and in vivo experiments.ResultsEndogenous MFG-E8 expression was downregulated in experimental AP. Genetic deletion of Mfge8 aggravated mitochondrial ultrastructural damage, impaired mitophagy flux and intensified ferroptosis, as evidenced by increased lipid peroxidation, Fe2+ accumulation and depletion of glutathione peroxidase. Lentiviral overexpression of MFG-E8 in AR42J acinar cells restored mitophagy activity, preserved mitochondrial membrane potential and reduced oxidative stress. Mechanistically, co-immunoprecipitation confirmed that MFG-E8 directly interacts with ABCE1, a key mitophagy regulator. ABCE1 knockdown abolished the protective effects of MFG-E8 on mitochondrial function and ferroptosis suppression, indicating that the MFG-E8/ABCE1 axis is essential for maintaining mitophagy homeostasis. Pharmacological restoration of mitophagy or inhibition of ferroptosis rescued acinar cell injury caused by MFG-E8/ABCE1 dysregulation. In vivo, ferroptosis inhibition significantly improved pancreatic pathology and survival in Mfge8-deficient AP mice.ConclusionEndogenous MFG-E8 protects against AP by binding ABCE1 to sustain mitophagy flux and inhibit ferroptosis. Targeting this axis offers a promising therapeutic strategy for mitigating pancreatic injury.Key pointsEndogenous MFG-E8 is downregulated in acute pancreatitis (AP), disrupting MFG-E8/ABCE1 complex formation. MFG-E8/ABCE1 axis sustains Parkin-PINK1-mediated mitophagy to clear damaged mitochondria in pancreatic acinar cells. This axis suppresses ferroptosis by reducing Fe2+ accumulation and lipid peroxidation, alleviating AP-related pancreatic injury.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41705299 · DOI · PMC12914346
Targeting mitochondrial phosphatase PGAM5 alleviates ferroptosis and acute pancreatitis by upregulating NRF2-mediated FSP1 expression [2]
Abstract reading summary — source excerpts
- Opening excerpt
- Ferroptosis is a regulated necrosis that is driven by iron-dependent lipid peroxidation.
- Closing excerpt
- The molecular mechanism of alleviation of ferroptosis by dysregulation of PGAM5.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (178 words)
Ferroptosis is a regulated necrosis that is driven by iron-dependent lipid peroxidation. Phosphoglycerate mutase 5 (PGAM5), as a mitochondrial signaling hub, modulates mitochondrial dynamics, senses mitochondrial stress, and regulates the anti-oxidative response. However, the function of PGAM5 in ferroptosis remains elusive. Here, we discovered that PGAM5 emerges as a critical regulator of ferroptosis, with both genetic deletion and overexpression conferring protection against ferroptosis by upregulating nuclear factor erythroid 2-related factor 2 (NRF2) mediated ferroptosis suppressor protein 1 (FSP1) expression. On the one hand, dyregulation of PGAM5 upregulates NRF2 expression transcriptionally and inhibits its polyubiquitination. On the other hand, modulating the expression of PGAM5 results in energy stress ([AMP + ADP]/[ATP] ratio increase) and AMP-activated protein kinase (AMPK) activation. AMPK-dependent phosphorylation of NRF2 drives its nuclear accumulation, where it transcriptionally upregulates FSP1 to promote cell survival. Furthermore, pharmacological inhibition of PGAM5 attenuates arginine-induced acute pancreatitis, highlighting its therapeutic potential. Our findings establish PGAM5 as a central node in ferroptosis regulation and implicate its pathogenic role in acute pancreatitis. The molecular mechanism of alleviation of ferroptosis by dysregulation of PGAM5.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41723122 · DOI · PMC12966488
Neutrophil extracellular traps prime the ZBP1-cGAS sensor complex, triggering necroptosis and inflammatory injury in acute pancreatitis [3]
Abstract reading summary — source excerpts
- Opening excerpt
- Severe acute pancreatitis (SAP) involves dynamic interactions between immune dysregulation and inflammatory infiltration.
- Closing excerpt
- Our findings establish the mtDNA-ZBP1-cGAS axis as a pivotal mechanism by which NETs exacerbate pancreatic inflammation, revealing new therapeutic targets for SAP.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (166 words)
Severe acute pancreatitis (SAP) involves dynamic interactions between immune dysregulation and inflammatory infiltration. Although elevated levels of neutrophil extracellular traps (NETs) are associated with SAP, the downstream mechanisms by which NETs exacerbate the inflammatory injury remain unclear. In this study, we demonstrate that NETs levels positively correlate with SAP severity, and pharmacological inhibition of NETs reduces pancreatic injury, and acinar cell death. Mechanistically, NETs activate the ZBP1-cGAS complex via mitochondrial DNA (mtDNA), triggering downstream necroptosis and inflammatory pathways, thereby driving pancreatic inflammatory injury. Specifically, NETs induce mitochondrial damage in acinar cells, leading to cytosolic accumulation of mtDNA. This recruits ZBP1 to form a complex with cGAS dependent on the RHIM domain, wherein ZBP1 stabilizes Z-form mtDNA and potentiates cGAS recognition of Z-mtDNA, thereby cooperatively promoting necroptosis and inflammation. Furthermore, cyclosporine A inhibits mtDNA release, thereby suppressing NETs-induced ZBP1-cGAS complex formation and mitigating pancreatic injury. Our findings establish the mtDNA-ZBP1-cGAS axis as a pivotal mechanism by which NETs exacerbate pancreatic inflammation, revealing new therapeutic targets for SAP.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41800237 · DOI · PMC12965145
Key reviews and meta-analyses
The most cited review-type papers among PubMed’s best-match results for this heading, listed with bibliographic details only. Follow the links for the full text and access terms.
- Research article Global Incidence of Acute Pancreatitis Is Increasing Over Time: A Systematic Review and Meta-Analysis [4]
- Research article Chronic Pancreatitis and Pancreatic Cancer Risk: A Systematic Review and Meta-analysis [5]
- Research article Appraising the causal role of smoking in multiple diseases: A systematic review and meta-analysis of Mendelian randomization studies [6]
- Research article Infection increases mortality in necrotizing pancreatitis: A systematic review and meta-analysis [7]
- Research article Pancreatic exocrine insufficiency following acute pancreatitis: Systematic review and study level meta-analysis [8]
- Research article Incidence, severity, and mortality of post-ERCP pancreatitis: an updated systematic review and meta-analysis of 145 randomized controlled trials [9]
Full-text reviews on EvidenceLib
Open-access review articles about this topic, reproduced in full with authors, licence and references.
Endoscopic versus surgical treatment for infected necrotizing pancreatitis: a systematic review and meta-analysis of randomized controlled trials
C M Haney, K F Kowalewski, M W Schmidt et al. · Surgical Endoscopy 2020 · CC BY 4.0
Aging and Comorbidities in Acute Pancreatitis I: A Meta-Analysis and Systematic Review Based on 194,702 Patients
Katalin Márta, Alina-Marilena Lazarescu, Nelli Farkas et al. · Frontiers in Physiology 2019 · CC BY 4.0
References
- Ren Y, Lu Y, Cui Q, Shang H, Fan M, Sun Y, et al.. Milk fat globule-EGF factor 8/ATP-binding cassette subfamily E member 1 axis maintains mitophagy flux homeostasis to suppress ferroptosis in acute pancreatitis. . 2026. PMID 41705299 · DOI · PMC12914346
- Ma S, Qin J, Luan J, Hou G, He J, Gao M. Targeting mitochondrial phosphatase PGAM5 alleviates ferroptosis and acute pancreatitis by upregulating NRF2-mediated FSP1 expression. . 2026. PMID 41723122 · DOI · PMC12966488
- Zhang H, Wang Z, Lu J, Li J, Jia Y, Xie X, et al.. Neutrophil extracellular traps prime the ZBP1-cGAS sensor complex, triggering necroptosis and inflammatory injury in acute pancreatitis. . 2026. PMID 41800237 · DOI · PMC12965145
- Iannuzzi JP, King JA, Leong JH, Quan J, Windsor JW, Tanyingoh D, et al.. Global Incidence of Acute Pancreatitis Is Increasing Over Time: A Systematic Review and Meta-Analysis. Gastroenterology. 2022. PMID 34571026 · DOI
- Kirkegård J, Mortensen FV, Cronin-Fenton D. Chronic Pancreatitis and Pancreatic Cancer Risk: A Systematic Review and Meta-analysis. Am J Gastroenterol. 2017. PMID 28762376 · DOI
- Larsson SC, Burgess S. Appraising the causal role of smoking in multiple diseases: A systematic review and meta-analysis of Mendelian randomization studies. EBioMedicine. 2022. PMID 35816897 · DOI · PMC9278068
- Werge M, Novovic S, Schmidt PN, Gluud LL. Infection increases mortality in necrotizing pancreatitis: A systematic review and meta-analysis. Pancreatology. 2016. PMID 27449605 · DOI
- Hollemans RA, Hallensleben NDL, Mager DJ, Kelder JC, Besselink MG, Bruno MJ, et al.. Pancreatic exocrine insufficiency following acute pancreatitis: Systematic review and study level meta-analysis. Pancreatology. 2018. PMID 29482892 · DOI
- Akshintala VS, Kanthasamy K, Bhullar FA, Sperna Weiland CJ, Kamal A, Kochar B, et al.. Incidence, severity, and mortality of post-ERCP pancreatitis: an updated systematic review and meta-analysis of 145 randomized controlled trials. Gastrointest Endosc. 2023. PMID 37004815 · DOI
About this article
- Sources
- NLM Medical Subject Headings (definition, synonyms); NCBI PubMed (counts, identifiers); Europe PMC (open-access abstracts and citation counts).
- Verification
- Every reference was resolved against PubMed on 2026-11-04; title, year and DOI matched.
- Review state
- automated source verified; no human expert review has been recorded yet.
- Version
- 1, last updated 2026-11-04.
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Evidence strength
EvidenceHelix's computed view of the study designs behind this topic: how common meta-analyses, randomized trials and reviews are, how recent the literature is, and a plain-language reading. It describes the design mix of the literature. It is not a quality appraisal of any study, and it is not medical advice.