ArticleGut2007
The neurotrophic factor artemin influences the extent of neural damage and growth in chronic pancreatitis.
Article in Gut, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers, 1 of them a synthesis that pooled it.
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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.
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Who cites it
56 citing papers in PubMed, 1 synthesis or guideline pooled it, 105 citations in OpenAlex.
- Treatment options in painful chronic pancreatitis: a systematic review.HPB : the official journal of the International Hepato Pancreato Biliary Association · 2014Pooled it
- Genetic evidence for causal link between systemic inflammation and dental caries risk: A bidirectional Mendelian randomization study.Medicine · 2026Article
- From Inflammation to Neuroplasticity: Molecular Mechanisms of Pain in Acute, Recurrent and Chronic Pancreatitis.International journal of molecular sciences · 2026Review
- Peripheral nerve remodeling in the tumor microenvironment: neuro-immune crosstalk, molecular mechanisms, and precision therapeutic.Frontiers in immunology · 2026Review
- Reprogramming neural-tumor crosstalk: emerging therapeutic dimensions and targeting strategies.Military Medical Research · 2025Review
- Emerging evidence of artemin/GFRα3 signaling in musculoskeletal pain.Osteoarthritis and cartilage · 2025Review
- Navigating chronic pancreatitis pain: a pathophysiological and therapeutic overview.Frontiers in physiology · 2025Review
- Neuropancreatology: The Nervous System and Pain Management in Pancreatic Diseases.Life (Basel, Switzerland) · 2024Review
- Neural innervation in adipose tissue, gut, pancreas, and liver.Life metabolism · 2023Review
- Review
- Targeting tumor innervation: premises, promises, and challenges.Cell death discovery · 2022Review
- Neuroimmunology of cancer and associated symptomology.Immunology and cell biology · 2021Review
- Nerve density in cancer: Less is better.FASEB bioAdvances · 2021Review
- CGRP-Mediated Prolactin Upregulation: a Possible Pathomechanism in IgG4-Related Disease.Inflammation · 2021Article
- Cancer-Associated Neurogenesis and Nerve-Cancer Cross-talk.Cancer research · 2021Review
- Severe Pain in Chronic Pancreatitis Patients: Considering Mental Health and Associated Genetic Factors.Journal of pain research · 2021Review
- ARTEMIN Promotes Oncogenicity and Resistance to 5-Fluorouracil in Colorectal Carcinoma by p44/42 MAPK Dependent Expression of CDH2.Frontiers in oncology · 2021Article
- Impaired autophagy increases susceptibility to endotoxin-induced chronic pancreatitis.Cell death & disease · 2020Article
- Glial cell line-derived neurotrophic factors (GFLs) and small molecules targeting RET receptor for the treatment of pain and Parkinson's disease.Cell and tissue research · 2020Review
- The role of glial cell line-derived neurotrophic factor family member artemin in neurological disorders and cancers.Cell proliferation · 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
11 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BACKGROUND AND
aimsChronic pancreatitis is characterised by severe abdominal neuropathic pain, perineural inflammatory cell infiltrations and intrapancreatic neural growth. Artemin was recently shown to eliminate neuropathic pain and reverse neurochemical damage after nerve injury. The role of artemin and its receptor GFRalpha3 was investigated in patients with chronic pancreatitis.
methodsExpression of artemin and its receptor GFRalpha3 was studied in chronic pancreatitis (n = 66) and normal (n = 22) pancreatic tissues by quantitative reverse transcription-polymerase chain reaction (QRT-PCR) and western blot analysis. Artemin expression was correlated with pain and pathomorphological changes (inflammation, perineural inflammatory cell infiltration, neural alterations and fibrosis). Immunohistochemistry was used to localise artemin and GFRalpha3 in the tissues. To detect sources of artemin, primary human pancreatic stellate cells (hPSCs) were isolated and analysed by QRT-PCR and immunocytology analysis.
resultsIn chronic pancreatitis, artemin and GFRalpha3 were significantly overexpressed and located in smooth muscle cells of arteries, Schwann cells and neural ganglia. Increased levels of artemin mRNA correlated with pain severity, inflammation, perineural inflammatory cell infiltration, neural density and hypertrophy. Furthermore, the severity of fibrosis was positively related with artemin expression and neural alterations. Activated hPSCs expressed low basal levels of artemin mRNA which were upregulated by exposure to transforming growth factor (TGF)beta1.
conclusionsOverexpression of artemin in chronic pancreatitis might function as a compensatory upregulation in order to repair neural damage incurred by ongoing pancreatic inflammation. Upregulation of TGFbeta1 seems not only to increase pancreatic fibrosis but also to contribute to neural alteration by stimulating artemin expression in hPSCs. However, overexpression of endogenous artemin does not seem to be sufficient to prevent pain in chronic pancreatitis.
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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.