ArticleMolecular and cellular biochemistry2022
TGF-β activates NLRP3 inflammasome by an autocrine production of TGF-β in LX-2 human hepatic stellate cells.
Article in Molecular and cellular biochemistry, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 36 citations in OpenAlex.
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- Targeting TGFBR1 with the Investigational Inhibitor TP-6379 Improves Hematopoiesis in Low-Risk MDS Ex Vivo.Cells · 2026Article
- Amphibian Skin-Derived Peptides as Emerging Therapeutic Scaffolds for Metabolic Dysfunction-Associated Steatotic Liver Disease (MASLD).Pharmaceuticals (Basel, Switzerland) · 2026Review
- Emerging role of FUS in TGFB1 and COL1A1 transcription dependent on GADD45B to induce NASH-fibrosis.Journal of molecular cell biology · 2026Article
- Impact of heatwave exposure on chronic kidney disease risk among middle-aged and older adults: evidence from the China health and retirement longitudinal study.BMC nephrology · 2026Article
- ISX-TWIST1 reprograms CD47-inflammasome signaling to reshape the immune microenvironment in liver cancer.Experimental hematology & oncology · 2026Article
- Diacerein improves liver fibrosis, steatosis, and atherosclerosis in ApoE knockout mice.Journal of molecular medicine (Berlin, Germany) · 2026Article
- Toll/IL-1 receptor domain-containing adaptor protein plays a crucial role in macrophage-mediated hepatic stellate cell activation in alcoholic liver disease.Frontiers in cell and developmental biology · 2026Article
- miRNA Expression Profile in Whole Blood of Healthy Volunteers and Moderate Beer Consumption with Meals.Nutrients · 2026Article
- Inhibition of TGF-beta signaling protects from alpha-synuclein induced toxicity.Cell death discovery · 2025Article
- Article
- The desulfinylation enzyme sulfiredoxin-1 attenuates HSC activation and liver fibrosis by modulating the PTPN12-NLRP3 axis.Hepatology (Baltimore, Md.) · 2025Article
- Dual signaling pathways of TGF-β superfamily cytokines in hepatocytes: balancing liver homeostasis and disease progression.Frontiers in pharmacology · 2025Review
- Novel approach to alleviate lupus nephritis: targeting the NLRP3 inflammasome in CD8Journal of translational medicine · 2024Article
- Crosstalk of pyroptosis and cytokine in the tumor microenvironment: from mechanisms to clinical implication.Molecular cancer · 2024Review
- Article
- Statin administration or blocking PCSK9 alleviates airway hyperresponsiveness and lung fibrosis in high-fat diet-induced obese mice.Respiratory research · 2024Article
- The miR-3074/BMP7 axis regulates TGF-β-caused activation of hepatic stellate cells in vitro and CClHuman cell · 2024Article
- Bystander Effects and Profibrotic Interactions in Hepatic Stellate Cells during HIV and HCV Coinfection.Journal of immunology research · 2024Article
- Selective Immunosuppression Targeting the NLRP3 Inflammasome Mitigates the Foreign Body Response to Implanted Biomaterials While Preserving Angiogenesis.Advanced healthcare materials · 2023Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Inflammation contributes to the pathogenesis of liver disease, and inflammasome activation has been identified as a major contributor to the amplification of liver inflammation. Transforming growth factor-beta (TGF-β) is a key regulator of liver physiology, contributing to all stages of liver disease. We investigated whether TGF-β is involved in inflammasome-mediated fibrosis in hepatic stellate cells. Treatment with TGF-β increased priming of NLRP3 inflammasome signaling by increasing NLRP3 levels and activating TAK1-NF-kB signaling. Moreover, TGF-β increased the expression of p-Smad2/3-NOX4 in LX-2 cells and consequently increased ROS content, which is a trigger for NLRP3 inflammasome activation. Elevated expression of NEK7 and active caspase-1 was also shown in TGF-β-induced LX-2 cells, and this level was reduced by (5Z)-oxozeaenol, a TAK inhibitor. Finally, TGF-β-treated cells significantly increased TGF-β secretion levels, and their production was inhibited by IL-1β receptor antagonist treatment. In conclusion, TGF-β may represent an endogenous danger signal to the active NLRP3 inflammasome, by which IL-1β mediates TGF-β expression in an autocrine manner. Therefore, targeting the NLRP3 inflammasome may be a promising approach for the development of therapies for TGF-β-induced liver fibrosis.
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