ArticleGastroenterology2018
Neuronal Transforming Growth Factor beta Signaling via SMAD3 Contributes to Pain in Animal Models of Chronic Pancreatitis.
Article in Gastroenterology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 49 citations in OpenAlex.
- Pain Hypersensitivity in a Mouse Model of Marfan Syndrome.Antioxidants (Basel, Switzerland) · 2026Article
- Peripheral Nerve-Cancer Interactions in the Tumor Microenvironment: A Three-Dimensional Framework Integrating Mechanisms, Modulators, and Therapeutic Strategies.Research (Washington, D.C.) · 2026Review
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- Master of innovation: unlocking creativity in the development of novel solutions from interventional endoscopy to neurogastroenterology.iGIE : innovation, investigation and insights · 2025Article
- Reprogramming neural-tumor crosstalk: emerging therapeutic dimensions and targeting strategies.Military Medical Research · 2025Review
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- miR-374 family is a key regulator of chronic primary pain onset.Pain reports · 2024Article
- Pancreatitis pain quality changes at year 1 follow-up, but GP130 remains a biomarker for pain.Pancreatology : official journal of the International Association of Pancreatology (IAP) ... [et al.] · 2024Article
- Persistent changes in nociceptor translatomes govern hyperalgesic priming in mouse models.bioRxiv : the preprint server for biology · 2024Article
- Recent advances in the understanding and management of chronic pancreatitis pain.Journal of pancreatology · 2024Review
- Serum Biomarkers of Nociceptive and Neuropathic Pain in Chronic Pancreatitis.The journal of pain · 2023Observational
- Krüppel-like Factor 5 Plays an Important Role in the Pathogenesis of Chronic Pancreatitis.Cancers · 2023Article
- Single-cell RNA sequencing uncovers a neuron-like macrophage subset associated with cancer pain.Science advances · 2022Article
- Transient receptor potential vanilloid subtype 1: A potential therapeutic target for fibrotic diseases.Frontiers in physiology · 2022Review
- Physiological Changes and Pathological Pain Associated with Sedentary Lifestyle-Induced Body Systems Fat Accumulation and Their Modulation by Physical Exercise.International journal of environmental research and public health · 2021Review
- Serum biomarkers for chronic pancreatitis pain patterns.Pancreatology : official journal of the International Association of Pancreatology (IAP) ... [et al.] · 2021Article
- Review
- Long non-coding RNA CDKN2B-AS1 enhances LPS-induced apoptotic and inflammatory damages in human lung epithelial cells via regulating the miR-140-5p/TGFBR2/Smad3 signal network.BMC pulmonary medicine · 2021Article
- Article
- Cardiopulmonary and Neurologic Dysfunctions in Fibrodysplasia Ossificans Progressiva.Biomedicines · 2021Review
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
Abstract
BACKGROUND &
aimsChronic pancreatitis (CP) is characterized by pancreatic inflammation and fibrosis, associated with increased pancreatic expression of transforming growth factor beta (TGFB). It is not clear how these might contribute to pain. We investigated whether TGFB signaling via SMAD induces sensitization of pancreatic sensory neurons to increase nociception.
methodsCP was induced in Sprague-Dawley rats by infusion of trinitrobenzene sulfonic acid; some rats were given intrathecal infusions of TGFB1. CP was induced in control mice by administration of cerulein; we also studied β1glo/Ptf1acre-ER mice, which on induction overexpress TGFB1 in pancreatic acinar cells, and TGFBr1
resultsOverexpression of TGFB in pancreatic acinar cells of mice and infusion of TGFB1 into rats resulted in sensory neuron hyperexcitability, SMAD3 activation, and increased nociception. This was accompanied by a reduction in the transient A-type current in pancreas-specific sensory neurons in rats, a characteristic of nociceptive sensitization in animal models of CP. Conversely, pancreata from TGFBr1
conclusionsIn pancreata of mice and rats, TGFB promotes peripheral nociceptive sensitization via a direct effect on primary sensory neurons mediated by intra-neuronal SMAD3. This is distinct from the central nervous system, where TGFB reduces nociception. These results provide an explanation for the link between fibrosis and pain in patients with CP. This signaling pathway might be targeted therapeutically to reduce pain in patients with CP.
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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.