ArticleInternational journal of molecular sciences2021
JNK and p38 Inhibitors Prevent Transforming Growth Factor-β1-Induced Myofibroblast Transdifferentiation in Human Graves' Orbital Fibroblasts.
Article in International journal of molecular sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 21 citations in OpenAlex.
- Gut Microbial Metabolite Indole-3-Acetic Acid Exerts Protective Effects by Regulating Orbital Fibroblast Fibrosis in Thyroid Eye Disease.Investigative ophthalmology & visual science · 2026Article
- The inflammatory-autophagy-NETs axis in renal fibrosis: mechanistic crosstalk and pathological feed-forward amplification loops.Molecular and cellular biochemistry · 2026Review
- Targeting canonical TGFβ/SMAD3 and ERK1/2 signaling in human valve interstitial cells to modulate immune-fibrotic responses in rheumatic heart disease.Journal of physiology and biochemistry · 2026Article
- Macrophage plasticity in thyroid eye disease: dual effects of inflammation and fibrosis.Frontiers in immunology · 2026Review
- Sea buckthorn flavonoids and their derivatives: potential natural compounds for the treatment of diabetic cardiomyopathy.Frontiers in pharmacology · 2025Review
- Endoplasmic reticulum protein TXNDC5 modulates thyroid eye disease TGF-β1-induced myofibroblast transdifferentiation.BMJ open ophthalmology · 2024Article
- Characteristics of Hyaluronan Metabolism During Myofibroblast Differentiation in Orbital Fibroblasts.Investigative ophthalmology & visual science · 2024Article
- An L-type calcium channel blocker nimodipine exerts anti-fibrotic effects by attenuating TGF-β1 induced calcium response in an in vitro model of thyroid eye disease.Eye and vision (London, England) · 2024Article
- A Review of Pathophysiology and Therapeutic Strategies Targeting TGF-β in Graves' Ophthalmopathy.Cells · 2024Review
- The Role of Fibrogenesis and Extracellular Matrix Proteins in the Pathogenesis of Graves' Ophthalmopathy.International journal of molecular sciences · 2024Review
- Ceruloplasmin regulating fibrosis in orbital fibroblasts provides a novel therapeutic target for Graves' orbitopathy.Journal of endocrinological investigation · 2023Article
- Connective tissue growth factor: Role in trabecular meshwork remodeling and intraocular pressure lowering.Experimental biology and medicine (Maywood, N.J.) · 2023Review
- Non-viral gene therapy using RNA interference with PDGFR-α mediated epithelial-mesenchymal transformation for proliferative vitreoretinopathy.Materials today. Bio · 2023Article
- First study on the effect of transforming growth factor beta 1 and insulin-like growth factor 1 on the chondrogenesis of elephant articular chondrocytes in a scaffold-based 3D culture model.Veterinary world · 2022Article
- SB203580-A Potent p38 MAPK Inhibitor Reduces the Profibrotic Bronchial Fibroblasts Transition Associated with Asthma.International journal of molecular sciences · 2021Article
- TGF-β3 regulates adhesion formation through the JNK/c-Jun pathway during flexor tendon healing.BMC musculoskeletal disorders · 2021Article
- Effect of Pirfenidone on TGF-β1-Induced Myofibroblast Differentiation and Extracellular Matrix Homeostasis of Human Orbital Fibroblasts in Graves' Ophthalmopathy.Biomolecules · 2021Article
- Ketamine Induced Bladder Fibrosis Through MTDH/P38 MAPK/EMT Pathway.Frontiers in pharmacology · 2021Article
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Transforming growth factor-β1 (TGF-β1)-induced myofibroblast transdifferentiation from orbital fibroblasts is known to dominate tissue remodeling and fibrosis in Graves' ophthalmopathy (GO). However, the signaling pathways through which TGF-β1 activates Graves' orbital fibroblasts remain unclear. This study investigated the role of the mitogen-activated protein kinase (MAPK) pathway in TGF-β1-induced myofibroblast transdifferentiation in human Graves' orbital fibroblasts. The MAPK pathway was assessed by measuring the phosphorylation of p38, c-Jun N-terminal kinase (JNK), and extracellular-signal-regulated kinase (ERK) by Western blots. The expression of connective tissue growth factor (CTGF), α-smooth muscle actin (α-SMA), and fibronectin representing fibrogenesis was estimated. The activities of matrix metalloproteinases (MMPs) and tissue inhibitors of metalloproteinases (TIMPs) responsible for extracellular matrix (ECM) metabolism were analyzed. Specific pharmacologic kinase inhibitors were used to confirm the involvement of the MAPK pathway. After treatment with TGF-β1, the phosphorylation levels of p38 and JNK, but not ERK, were increased. CTGF, α-SMA, and fibronectin, as well as TIMP-1 and TIMP-3, were upregulated, whereas the activities of MMP-2/-9 were inhibited. The effects of TGF-β1 on the expression of these factors were eliminated by p38 and JNK inhibitors. The results suggested that TGF-β1 could induce myofibroblast transdifferentiation in human Graves' orbital fibroblasts through the p38 and JNK pathways.
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Registered trials
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