ReviewPhilosophical transactions of the Royal Society of London. Series B, Biological sciences2016
Ca2+ toxicity and mitochondrial damage in acute pancreatitis: translational overview.
Review in Philosophical transactions of the Royal Society of London. Series B, Biological sciences, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers, 3 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
52 citing papers in PubMed, 3 syntheses or guidelines pooled it, 87 citations in OpenAlex.
- AEG-AESPANC-OPGE-SIED-SPG Ibero-Latin American Guidelines on Acute Pancreatitis (iLATAM-AP).United European gastroenterology journal · 2026Guideline
- Restoration of energy level in the early phase of acute pediatric pancreatitis.World journal of gastroenterology · 2017Pooled it
- Pooled it
- Trial
- Cell death and its interaction with mitochondrial dysfunction in pathogenesis of acute pancreatitis: a comprehensive review.Apoptosis : an international journal on programmed cell death · 2026Review
- Nanotherapy for Pancreatitis: From Single-Cell Targeting Toward Multicellular-Coordinated Regulation.International journal of nanomedicine · 2026Review
- Targeted therapeutics for pancreatitis.Frontiers in physiology · 2026Review
- The association of arterial partial oxygen pressure with mortality in patients with severe acute pancreatitis: a retrospective cohort study.Intensive care medicine experimental · 2025Article
- Pancreatic involvement inMolecular genetics and metabolism reports · 2025Article
- Calumenin, A Calcium-Binding Modulatory Protein, Effective in Pathological Calcifications and Cancers, With Therapeutic Application Promise.FASEB bioAdvances · 2025Review
- Targeting Oxidative Stress in Acute Pancreatitis: A Critical Review of Antioxidant Strategies.Nutrients · 2025Review
- Cerium-based nanoplatform for severe acute pancreatitis: Achieving enhanced anti-inflammatory effects through calcium homeostasis restoration and oxidative stress mitigation.Materials today. Bio · 2025Article
- Pentraxin3 exacerbates acute pancreatitis injury by inhibiting oxidative phosphorylation pathway.Scientific reports · 2025Article
- Deletion of the WD40 domain of ATG16L1 exacerbates acute pancreatitis, abolishes LAP-like non-canonical autophagy and slows trypsin degradation.Autophagy · 2025Article
- Review
- Natural Compounds for the Treatment of Acute Pancreatitis: Novel Anti-Inflammatory Therapies.Biomolecules · 2024Review
- Oxidative stress and acute pancreatitis (Review).Biomedical reports · 2024Review
- Identifying novel acute pancreatitis sub-phenotypes using total serum calcium trajectories.BMC gastroenterology · 2024Article
- Elimination of intracellular CaInternational journal of molecular medicine · 2024Article
- Isorhamnetin Alleviates Mitochondrial Injury in Severe Acute Pancreatitis via Modulation of KDM5B/HtrA2 Signaling Pathway.International journal of molecular sciences · 2024Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Acute pancreatitis (AP) is a leading cause of hospitalization among non-malignant gastrointestinal disorders. The mortality of severe AP can reach 30-50%, which is most probably owing to the lack of specific treatment. Therefore, AP is a major healthcare problem, which urges researchers to identify novel drug targets. Studies from the last decades highlighted that the toxic cellular Ca(2+) overload and mitochondrial damage are key pathogenic steps in the disease development affecting both acinar and ductal cell functions. Moreover, recent observations showed that modifying the cellular Ca(2+) signalling might be beneficial in AP. The inhibition of Ca(2+) release from the endoplasmic reticulum or the activity of plasma membrane Ca(2+) influx channels decreased the severity of AP in experimental models. Similarly, inhibition of mitochondrial permeability transition pore (MPTP) opening also seems to improve the outcome of AP in in vivo animal models. At the moment MPTP blockers are under detailed clinical investigation to test whether interventions in MPTP openings and/or Ca(2+) homeostasis of the cells can be specific targets in prevention or treatment of cell damage in AP.This article is part of the themed issue 'Evolution brings Ca(2+) and ATP together to control life and death'.
Indexed as
Identifiers
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.