ArticleMolecular and cellular biochemistry2015
Smad2 protects against TGF-β1/Smad3-mediated collagen synthesis in human hepatic stellate cells during hepatic fibrosis.
Article in Molecular and cellular biochemistry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 71 citations in OpenAlex.
- PLCε regulates podocyte differentiation and TGF-β1 responses via alteration of SMAD2/SMAD3 ratio.Cell communication and signaling : CCS · 2026Article
- Antagonistic SMAD2/3 control of TIMP-1, VEGF-A, and hypoxia signaling in myofibroblasts shapes histotype-specific angiogenesis in lung cancer.Cell death & disease · 2026Article
- Proteomic analysis of 7-octenoic acid antifibrotic effects in TGF-β1 activated hepatic stellate cells.Scientific reports · 2025Article
- The pivotal role of TGF-β/Smad pathway in fibrosis pathogenesis and treatment.Frontiers in oncology · 2025Review
- Exploring the Antifibrotic Mechanisms of Ghrelin: Modulating TGF-β Signalling in Organ Fibrosis.Expert reviews in molecular medicine · 2024Review
- Investigating the Antifibrotic Effects of β-Citronellol on a TGF-β1-Stimulated LX-2 Hepatic Stellate Cell Model.Biomolecules · 2024Article
- The miR-3074/BMP7 axis regulates TGF-β-caused activation of hepatic stellate cells in vitro and CClHuman cell · 2024Article
- CLC-3 regulates TGF-β/smad signaling pathway to inhibit the process of fibrosis in hypertrophic scar.Heliyon · 2024Article
- Loss of Krüppel-like factor-10 facilitates the development of chemical-induced liver cancer in mice.Molecular medicine (Cambridge, Mass.) · 2023Article
- Extracellular matrix remodelling in obesity and metabolic disorders.Life metabolism · 2023Article
- Krüppel-like factor 10 (KLF10) as a critical signaling mediator: Versatile functions in physiological and pathophysiological processes.Genes & diseases · 2023Review
- Hepatic stellate cell-intrinsic role of SOCS1 in controlling hepatic fibrogenic response and the pro-inflammatory macrophage compartment during liver fibrosis.Frontiers in immunology · 2023Article
- Sulforaphane prevents and reverses allergic airways disease in mice via anti-inflammatory, antioxidant, and epigenetic mechanisms.Cellular and molecular life sciences : CMLS · 2022Article
- The Role of Mesothelin in Activation of Portal Fibroblasts in Cholestatic Liver Injury.Biology · 2022Review
- Dietary protein levels changed the hardness of muscle by acting on muscle fiber growth and the metabolism of collagen in sub-adult grass carp (Ctenopharyngodon idella).Journal of animal science and biotechnology · 2022Article
- Pathophysiological communication between hepatocytes and non-parenchymal cells in liver injury from NAFLD to liver fibrosis.Advanced drug delivery reviews · 2021Review
- Mesenchymal Stem Cells Therapies on Fibrotic Heart Diseases.International journal of molecular sciences · 2021Review
- Adipocyte Fatty Acid Binding Protein Promotes the Onset and Progression of Liver Fibrosis via Mediating the Crosstalk between Liver Sinusoidal Endothelial Cells and Hepatic Stellate Cells.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2021Article
- Gasotransmitters: Potential Therapeutic Molecules of Fibrotic Diseases.Oxidative medicine and cellular longevity · 2021Review
- Antifibrotic Effects of Kangxian Ruangan Capsule on Rats with Nonalcoholic Fatty Liver Fibrosis and Hepatic Stellate Cells through Regulation of TGF-Evidence-based complementary and alternative medicine : eCAM · 2021Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
With structural similarity but functional diversity, Smad2 and Smad3 interact with each other to mediate transforming growth factor-β (TGF-β)-triggered signaling transduction. However, in the hepatic fibrosis, the detailed roles of R-Smads, and interaction between Smad2 and Smad3 are still undefined. In this setting, we established a rat model of CCl4-induced hepatic fibrosis in vivo and TGF-β1-treated hepatic stellate cell model in vitro to detect whether Smad2 and Smad3 play distinct roles in mediating liver fibrogenesis. Results indicated that both phosphorylation of Smad2 and Smad3 were detected in the hepatic stellate cells of liver fibrotic tissues and cells. Furthermore, In vitro data demonstrated that knockdown of Smad2 in human hepatic stellate cells increased expression of collagen I (Col.I), tissue inhibitor of metalloproteinase-1 (TIMP-1) whereas decreasing expression of the matrix metalloproteinases-2(MMP-2) in presence of TGF-β1 compared with control group. In contrast, knockdown of Smad3 significantly reduced TGF-β1-induced Col.I production. These findings were further evident by the results that overexpression of Smad2 attenuated the expression of Col.I and TIMP-1, but enhanced MMP-2 whereas overexpression of Smad3 showed the opposite effect. Furthermore, Smad2 suppressed the phosphorylation and nuclear translocation of Smad3, which may protect against Smad3-mediated fibrotic response. Collectively, Smad2 may be a potential therapeutic target for the treatment of hepatic fibrosis.
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