ReviewThe Journal of physiology2014
The role of Ca2+ in the pathophysiology of pancreatitis.
Review in The Journal of physiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 85 papers, 2 of them syntheses that pooled it.
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
85 citing papers in PubMed, 2 syntheses or guidelines pooled it, 141 citations in OpenAlex.
- The relationship between different dimensions of alcohol use and the burden of disease-an update.Addiction (Abingdon, England) · 2017Pooled it
- Alcohol Consumption as a Risk Factor for Acute and Chronic Pancreatitis: A Systematic Review and a Series of Meta-analyses.EBioMedicine · 2015Pooled it
- Mechanistic insights into Orai dynamics during pore opening.Channels (Austin, Tex.) · 2026Review
- Modulation of Pancreatic Activity by Ghrelin and Its Potential Effects on Acute Pancreatitis.Digestive diseases and sciences · 2026Review
- Interpretable machine learning model based on non-contrast computed tomography within 24 hours of admission for early prediction of the risk of severe deterioration of acute pancreatitis.Quantitative imaging in medicine and surgery · 2026Article
- Hypertriglyceridaemia-Associated Acute Pancreatitis: Pathophysiological Insights and Advances in Clinical Management.Biomedicines · 2026Review
- Breaking the Calcium Overload Cycle in Acute Pancreatitis: Emerging Pharmacological Strategies.Digestive diseases and sciences · 2026Review
- Loss of the ER-cargo protein CLN8 increases severity of acute pancreatitis and upregulates ER-stress and ER-phagy.Molecular biomedicine · 2026Article
- BCL2 inhibition in acute and chronic pancreatitis - is there a therapeutic perspective?Cell death discovery · 2026Review
- Nanotherapy for Pancreatitis: From Single-Cell Targeting Toward Multicellular-Coordinated Regulation.International journal of nanomedicine · 2026Review
- Correlation of hypercalcemia with kidney stone formation and calcium-regulating hormone changes in patients with acute pancreatitis.World journal of gastrointestinal surgery · 2025Article
- Review
- Pancreatic involvement inMolecular genetics and metabolism reports · 2025Article
- 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
- Trypsin in pancreatitis: The culprit, a mediator, or epiphenomenon?World journal of gastroenterology · 2024Review
- Article
- Oxidative stress and acute pancreatitis (Review).Biomedical reports · 2024Review
- Bile Acids in Pancreatic Carcinogenesis.Metabolites · 2024Review
25 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
3 authors at 1 institution in 1 country.
Funding
Abstract
Acute pancreatitis is a human disease in which the pancreatic pro-enzymes, packaged into the zymogen granules of acinar cells, become activated and cause autodigestion. The main causes of pancreatitis are alcohol abuse and biliary disease. A considerable body of evidence indicates that the primary event initiating the disease process is the excessive release of Ca(2+) from intracellular stores, followed by excessive entry of Ca(2+) from the interstitial fluid. However, Ca(2+) release and subsequent entry are also precisely the processes that control the physiological secretion of digestive enzymes in response to stimulation via the vagal nerve or the hormone cholecystokinin. The spatial and temporal Ca(2+) signal patterns in physiology and pathology, as well as the contributions from different organelles in the different situations, are therefore critical issues. There has recently been significant progress in our understanding of both physiological stimulus-secretion coupling and the pathophysiology of acute pancreatitis. Very recently, a promising potential therapeutic development has occurred with the demonstration that the blockade of Ca(2+) release-activated Ca(2+) currents in pancreatic acinar cells offers remarkable protection against Ca(2+) overload, intracellular protease activation and necrosis evoked by a combination of alcohol and fatty acids, which is a major trigger of acute pancreatitis.
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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.