ReviewAnnual review of physiology2015
Regeneration and repair of the exocrine pancreas.
Review in Annual review of physiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 106 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
106 citing papers in PubMed, 2 syntheses or guidelines pooled it, 193 citations in OpenAlex.
- MiRNA-loaded MSC exosomes restore autophagy flux for acute pancreatitis therapy.Frontiers in immunology · 2025Pooled it
- Exocrine Pancreatic Insufficiency Following Acute Pancreatitis: Systematic Review and Meta-Analysis.Digestive diseases and sciences · 2019Pooled it
- Proteomic Insights into Molybdenum-Induced Pancreatic Injury in Goats.Biological trace element research · 2026Article
- Multi-stromal organoid co-culture modelling reveals epithelial-fibroblast heterogeneity in pancreatic cancer and pancreatitis.Nature cell biology · 2026Article
- Cyclin C promotes pancreatic developmentand suppresses cancer initiation by maintenance of the autophagy-lysosome pathway.iScience · 2026Article
- An Updated Narrative Review on the Therapeutic Potential of Resveratrol in the Treatment of Cancer.Health science reports · 2026Article
- AXL and MERTK facilitate tissue repair in severe acute pancreatitis via a CCR5-dependent neutrophil and macrophage crosstalk.Cell communication and signaling : CCS · 2025Article
- RalGAP complexes control secretion and primary cilia in pancreatic disease.Life science alliance · 2025Article
- Stromal Cells in Early Inflammation-Related Pancreatic Carcinogenesis-Biology and Its Potential Role in Therapeutic Targeting.Cancers · 2025Review
- Inhibition of hedgehog signaling ameliorates severity of chronic pancreatitis in experimental mouse models.American journal of physiology. Gastrointestinal and liver physiology · 2025Article
- Therapeutic potential of garlic, aged garlic extract and garlic‑derived compounds on pancreatic cancer (Review).Biomedical reports · 2025Review
- LRG1 inhibition promotes acute pancreatitis recovery by inducing cholecystokinin Type 1 receptor expression via Akt.Theranostics · 2025Article
- Article
- Engineered tools to study endocrine dysfunction of pancreas.Biophysics reviews · 2024Review
- Botanical drugs and their natural compounds: a neglected treasury for inhibiting the carcinogenesis of pancreatic ductal adenocarcinoma.Pharmaceutical biology · 2024Review
- FRA1 controls acinar cell plasticity during murine KrasDevelopmental cell · 2024Article
- Alterations in exocrine pancreatic function after acute pancreatitis.Pancreatology : official journal of the International Association of Pancreatology (IAP) ... [et al.] · 2024Review
- Article
- Protein kinase D1 - A targetable mediator of pancreatic cancer development.Biochimica et biophysica acta. Molecular cell research · 2024Review
- Ion channels in acinar cells in acute pancreatitis: crosstalk of calcium, iron, and copper signals.Frontiers in immunology · 2024Review
46 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
2 authors at 1 institution in 1 country.
Funding
Abstract
Pancreatitis is caused by inflammatory injury to the exocrine pancreas, from which both humans and animal models appear to recover via regeneration of digestive enzyme-producing acinar cells. This regenerative process involves transient phases of inflammation, metaplasia, and redifferentiation, driven by cell-cell interactions between acinar cells, leukocytes, and resident fibroblasts. The NFκB signaling pathway is a critical determinant of pancreatic inflammation and metaplasia, whereas a number of developmental signals and transcription factors are devoted to promoting acinar redifferentiation after injury. Imbalances between these proinflammatory and prodifferentiation pathways contribute to chronic pancreatitis, characterized by persistent inflammation, fibrosis, and acinar dedifferentiation. Loss of acinar cell differentiation also drives pancreatic cancer initiation, providing a mechanistic link between pancreatitis and cancer risk. Unraveling the molecular bases of exocrine regeneration may identify new therapeutic targets for treatment and prevention of both of these deadly diseases.
Indexed as
Identifiers
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.