ReviewWorld journal of gastroenterology2014
Calcium signaling of pancreatic acinar cells in the pathogenesis of pancreatitis.
Review in World journal of gastroenterology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers, 2 of them syntheses that pooled it.
What it found
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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
30 citing papers in PubMed, 2 syntheses or guidelines pooled it, 56 citations in OpenAlex.
- MiRNA-loaded MSC exosomes restore autophagy flux for acute pancreatitis therapy.Frontiers in immunology · 2025Pooled it
- Heavy Coffee Consumption and Risk of Pancreatitis: A Systematic Review and Meta-Analysis.Digestive diseases and sciences · 2018Pooled it
- Rhein alleviates acute pancreatitis by inhibiting TMAO-mediated inflammatory signaling pathways and reducing acinar cell injury.Journal of advanced research · 2026Article
- Acute pancreatitis: mechanisms and therapeutic approaches.Signal transduction and targeted therapy · 2026Review
- Mitochondrial dysfunction as a bridge to pathology in acute pancreatitis: From molecular insights to novel therapeutic strategies.World journal of gastroenterology · 2025Review
- Acinar-derived VEGF-A orchestrates blood vascular remodeling and preserves microvessels during acute pancreatitis.Cell communication and signaling : CCS · 2025Article
- Upregulation of ELP3 in acinar cells during acute pancreatitis is dispensable for homeostasis, inflammation, regeneration, and cancer initiation.Scientific reports · 2025Article
- Free and Bioavailable Vitamin D Are Correlated with Disease Severity in Acute Pancreatitis: A Single-Center, Prospective Study.International journal of molecular sciences · 2025Article
- Novel impact of metal ion-induced cell death on diabetic cardiomyopathy pathogenesis and therapy.Apoptosis : an international journal on programmed cell death · 2025Review
- Evaluation of scoring systems and hematological parameters in the severity stratification of early-phase acute pancreatitis.World journal of gastroenterology · 2025Observational
- Bioactive Nanomaterials: Comprehensive Monitoring and Regulation of Acute Pancreatitis Induced Acute Lung Injury.International journal of nanomedicine · 2025Review
- Review
- Bile Acids in Pancreatic Carcinogenesis.Metabolites · 2024Review
- Elimination of intracellular CaInternational journal of molecular medicine · 2024Article
- Mitochondrial dysfunction in pancreatic acinar cells: mechanisms and therapeutic strategies in acute pancreatitis.Frontiers in immunology · 2024Review
- Article
- Early prediction of acute necrotizing pancreatitis by artificial intelligence: a prospective cohort-analysis of 2387 cases.Scientific reports · 2022Article
- New insights into the etiology, risk factors, and pathogenesis of pancreatitis in dogs: Potential impacts on clinical practice.Journal of veterinary internal medicine · 2022Review
- Article
- Proteomic and Bioinformatic Analysis of Decellularized Pancreatic Extracellular Matrices.Molecules (Basel, Switzerland) · 2021Article
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
No grant is acknowledged in the PubMed record.
Abstract
Pancreatitis is an increasingly common and sometimes severe disease that lacks a specific therapy. The pathogenesis of pancreatitis is still not well understood. Calcium (Ca(2+)) is a versatile carrier of signals regulating many aspects of cellular activity and plays a central role in controlling digestive enzyme secretion in pancreatic acinar cells. Ca(2+) overload is a key early event and is crucial in the pathogenesis of many diseases. In pancreatic acinar cells, pathological Ca(2+) signaling (stimulated by bile, alcohol metabolites and other causes) is a key contributor to the initiation of cell injury due to prolonged and global Ca(2+) elevation that results in trypsin activation, vacuolization and necrosis, all of which are crucial in the development of pancreatitis. Increased release of Ca(2+) from stores in the intracellular endoplasmic reticulum and/or increased Ca(2+) entry through the plasma membrane are causes of such cell damage. Failed mitochondrial adenosine triphosphate (ATP) production reduces re-uptake and extrusion of Ca(2+) by the sarco/endoplasmic reticulum Ca(2+)-activated ATPase and plasma membrane Ca(2+)-ATPase pumps, which contribute to Ca(2+) overload. Current findings have provided further insight into the roles and mechanisms of abnormal pancreatic acinar Ca(2+) signals in pancreatitis. The lack of available specific treatments is therefore an objective of ongoing research. Research is currently underway to establish the mechanisms and interactions of Ca(2+) signals in the pathogenesis of pancreatitis.
Indexed as
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What Socratic 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 Socratic graph.