ReviewJournal of gastroenterology2008
Mechanisms of pancreatic fibrosis and applications to the treatment of chronic pancreatitis.
Review in Journal of gastroenterology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 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
53 citing papers in PubMed, 105 citations in OpenAlex.
- Analyzing the effect of neoadjuvant stereotactic ablative body radiotherapy on pancreatic tumor perfusion using computed tomography perfusion.Frontiers in oncology · 2026Article
- Targeted therapeutics for pancreatitis.Frontiers in physiology · 2026Review
- Fibrosis and cancer intersection.Journal of translational medicine · 2025Article
- SLC7A11 in Fibrosis: Molecular Mechanisms and Future Prospects.Aging and disease · 2025Review
- Pancreatic endocrine and exocrine signaling and crosstalk in physiological and pathological status.Signal transduction and targeted therapy · 2025Review
- Therapeutic potential of traditional Chinese medicine in pancreatic fibrosis: mechanisms of TCM formulas and active ingredients.Frontiers in pharmacology · 2025Review
- Elucidating the Role of Pro-renin Receptors in Pancreatic Ductal Adenocarcinoma Progression: A Novel Therapeutic Target in Cancer Therapy.Current cancer drug targets · 2024Review
- Differential location of growth factors and pancreatic stellate cell activation in chronic pancreatitis.Indian journal of gastroenterology : official journal of the Indian Society of Gastroenterology · 2023Article
- GPCRs and fibroblast heterogeneity in fibroblast-associated diseases.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2023Review
- Pancreatic Stellate Cells and the Targeted Therapeutic Strategies in Chronic Pancreatitis.Molecules (Basel, Switzerland) · 2023Review
- Fibrosis in Liver and Pancreas: a Review on Pathogenic Significance, Diagnostic Options, and Current Management Strategies.Inflammation · 2023Review
- Repetitive Cerulein-Induced Chronic Pancreatitis in Growing Pigs-A Pilot Study.International journal of molecular sciences · 2023Article
- Mechanotransductive receptorFrontiers in molecular biosciences · 2023Review
- Nutritional Support in Pancreatic Diseases.Nutrients · 2022Review
- Resistance to Gemcitabine in Pancreatic Ductal Adenocarcinoma: A Physiopathologic and Pharmacologic Review.Cancers · 2022Review
- Article
- TGFB1/INHBA Homodimer/Nodal-SMAD2/3 Signaling Network: A Pivotal Molecular Target in PDAC Treatment.Molecular therapy : the journal of the American Society of Gene Therapy · 2021Review
- The effects of nuclear factor-kappa B in pancreatic stellate cells on inflammation and fibrosis of chronic pancreatitis.Journal of cellular and molecular medicine · 2021Article
- Article
- Selective phytochemicals targeting pancreatic stellate cells as new anti-fibrotic agents for chronic pancreatitis and pancreatic cancer.Acta pharmaceutica Sinica. B · 2020Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Pancreatic stellate cells (PSCs) play a crucial role in pancreatic fibrogenesis in chronic pancreatitis and in the desmoplastic reaction of pancreatic cancer. When PSCs are stimulated by oxidative stress, ethanol and its metabolite acetaldehyde, and cytokines, the phenotype of quiescent fat-storing cells converts to myofibroblastlike activated PSCs, which then produce extracellular matrix, adhesion molecules, and various chemokines in response to cytokines and growth factors. Recent data suggest that PSCs have a phagocytic function. Plateletderived growth factor is a potent stimulator of PSC proliferation. Transforming growth factor beta, activin A, and connective tissue growth factor also play a role in PSC-mediated pancreatic fibrogenesis through autocrine and paracrine loops. Following pancreatic damage, pathophysiological processes that occur in the pancreas, including pancreas tissue pressure, hyperglycemia, intracellular reactive oxygen species production, activation of protease-activated receptor 2, induction of cyclooxygenase 2, and bacterial infection play a role in sustaining pancreatic fibrosis through increased PSC proliferation and collagen production by PSCs. Targeting PSCs might be an effective therapeutic approach in chronic pancreatitis. Various substances including vitamin A, vitamin E, polyphenols, peroxisome proliferator-activated receptor gamma ligands, and inhibitors of the renin-angiotensin system show great promise of being useful in the treatment of chronic pancreatitis.
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.