ArticleJournal of cellular and molecular medicine2021
The effects of nuclear factor-kappa B in pancreatic stellate cells on inflammation and fibrosis of chronic pancreatitis.
Article in Journal of cellular and molecular medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 42 citations in OpenAlex.
- Interruption of cross-communication pathways alters the immune cell signature of pancreatic cancer and decreases tumor growth.Cell communication and signaling : CCS · 2026Article
- Review
- Collagen Signaling via DDR1 Exacerbates Barriers to Macromolecular Drug Delivery in a 3D Model of Pancreatic Cancer Fibrosis.Small (Weinheim an der Bergstrasse, Germany) · 2025Article
- Notch3 enhances the synergistic effect of all-trans retinoic acid and calcipotriol in pancreatic stellate cell activation.Journal of translational medicine · 2025Article
- Metabolism and Targeted Therapy of Fibrosis in Chronic Pancreatitis: A Review.International journal of medical sciences · 2025Review
- Combination of Botanicals and Mindfulness Meditation for the Treatment of Chronic Pancreatitis: A Case Report.Journal of chiropractic medicine · 2025Article
- The Effects of Da-Chai-Hu Decoction Alleviating Pancreatic Exocrine Dysfunction by Inhibiting Endoplasmic Reticulum Stress of Acinar Cell in Mice with Chronic Pancreatitis.Journal of inflammation research · 2025Article
- Pancreatic stellate cells: Key players in pancreatic health and diseases (Review).Molecular medicine reports · 2024Review
- Fibroblast subtypes in pancreatic cancer and pancreatitis: from mechanisms to therapeutic strategies.Cellular oncology (Dordrecht, Netherlands) · 2024Review
- Activation and Regulation of Pancreatic Stellate Cells in Chronic Pancreatic Fibrosis: A Potential Therapeutic Approach for Chronic Pancreatitis.Biomedicines · 2024Review
- The role and therapeutic targeting of the CCL2/CCR2 signaling axis in inflammatory and fibrotic diseases.Frontiers in immunology · 2024Review
- Pancreatic Stellate Cells and the Targeted Therapeutic Strategies in Chronic Pancreatitis.Molecules (Basel, Switzerland) · 2023Review
- Immune response mechanisms in acute and chronic pancreatitis: strategies for therapeutic intervention.Frontiers in immunology · 2023Review
- Targeting pancreatic stellate cells in chronic pancreatitis: Focus on therapeutic drugs and natural compounds.Frontiers in pharmacology · 2022Review
- Pancreatic stellate cells - rising stars in pancreatic pathologies.Physiological research · 2021Review
- Long non-coding RNA NORAD promotes pancreatic cancer stem cell proliferation and self-renewal by blocking microRNA-202-5p-mediated ANP32E inhibition.Journal of translational medicine · 2021Article
- 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
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
Abstract
The activation of pancreatic stellate cells (PSCs) plays a critical role in the progression of pancreatic fibrosis. Nuclear factor-kappa B (NF-κB) is associated with chronic pancreatitis (CP). Previous evidence indicated that NF-κB in acinar cells played a double-edged role upon pancreatic injury, whereas NF-κB in inflammatory cells promoted the progression of CP. However, the effects of NF-κB in PSCs have not been studied. In the present study, using two CP models and RNAi strategy of p65 in cultured PSCs, we found that the macrophage infiltration and MCP-1 expression were increased, and the NF-κBp65 protein level was elevated. NF-κBp65 was co-expressed with PSCs. In vitro, TGF-β1 induced overexpression of the TGF-β receptor 1, phosphorylated TGF-β1-activated kinase 1 (p-TAK1) and NF-κB in the PSCs. Moreover, the concentration of MCP-1 in the supernatant of activated PSCs was elevated. The migration of BMDMs was promoted by the supernatant of activated PSCs. Further knockdown of NF-κBp65 in PSCs resulted in a decline of BMDM migration, accompanied by a lower production of MCP-1. These findings indicate that TGF-β1 can induce the activation of NF-κB pathway in PSCs by regulating p-TAK1, and the NF-κB pathway in PSCs may be a target of chronic inflammation and fibrosis.
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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.