ReviewCurrent opinion in gastroenterology2010
Molecular and cellular mechanisms of pancreatic injury.
Review in Current opinion in gastroenterology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 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
16 citing papers in PubMed, 65 citations in OpenAlex.
- Nirmatrelvir-Ritonavir-Induced Pancreatitis: A Concern in the COVID Era.ACG case reports journal · 2026Article
- Vitamin B6 ameliorates acute pancreatitis by suppressing the caspase3 signaling pathway.BMC gastroenterology · 2024Article
- Elevated intracellular trypsin exacerbates acute pancreatitis and chronic pancreatitis in mice.American journal of physiology. Gastrointestinal and liver physiology · 2019Article
- Intravenous injection of post-hemorrhagic shock mesenteric lymph induces multiple organ injury in rats.Experimental and therapeutic medicine · 2019Article
- Alcohol sedation in adultCommunications biology · 2019Article
- Animal models of gastrointestinal and liver diseases. Animal models of acute and chronic pancreatitis.American journal of physiology. Gastrointestinal and liver physiology · 2016Review
- PRSS1 mutations and the proteinase/antiproteinase imbalance in the pathogenesis of pancreatic cancer.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016Article
- Pharmacological attenuation of chronic alcoholic pancreatitis induced hypersensitivity in rats.World journal of gastroenterology · 2015Article
- Mesenteric lymph drainage alleviates acute kidney injury induced by hemorrhagic shock without resuscitation.TheScientificWorldJournal · 2014Article
- Flavocoxid, a nutraceutical approach to blunt inflammatory conditions.Mediators of inflammation · 2014Review
- Pancreatitis activates pancreatic apelin-APJ axis in mice.American journal of physiology. Gastrointestinal and liver physiology · 2013Article
- Alcohol consumption on pancreatic diseases.World journal of gastroenterology · 2013Review
- Genetics of pancreatitis: an update for clinicians and genetic counselors.Current gastroenterology reports · 2012Review
- Zymophagy: selective autophagy of secretory granules.International journal of cell biology · 2012Article
- Trypsin reduces pancreatic ductal bicarbonate secretion by inhibiting CFTR Cl⁻ channels and luminal anion exchangers.Gastroenterology · 2011Article
- TMAO promotes apoptosis and oxidative stress of pancreatic acinar cells by mediating IRE1α-XBP-1 pathway.Saudi journal of gastroenterology : official journal of the Saudi Gastroenterology AssociationArticle
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 2 institutions in 1 country.
Funding
Abstract
purpose of reviewThis review focuses on studies from the past year that highlight molecular and cellular mechanisms of pancreatic injury arising from acute and chronic pancreatitis. RECENT
findingsFactors that induce or ameliorate injury as well as cellular pathways involved have been examined. Causative or sensitizing factors include refluxed bile acids, hypercalcemia, ethanol, hypertriglyceridemia, and acidosis. In addition, the diabetes drug exendin-4 has been associated with pancreatitis, whereas other drugs may reduce pancreatic injury. The intracellular events that influence disease severity are better understood. Cathepsin-L promotes injury through an antiapoptotic effect, rather than by trypsinogen activation. In addition, specific trypsinogen mutations lead to trypsinogen misfolding, endoplasmic reticulum stress, and injury. Endogenous trypsin inhibitors and upregulation of proteins including Bcl-2, fibroblast growth factor 21, and activated protein C can reduce injury. Immune cells, however, have been shown to increase injury via an antiapoptotic effect. SUMMARY: The current findings are critical to understanding how causative factors initiate downstream cellular events resulting in pancreatic injury. Such knowledge will aid in the development of targeted treatments for pancreatitis. This review will first discuss factors influencing pancreatic injury, and then conclude with studies detailing the cellular mechanisms involved.
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.