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Found 16 results

  1. PU.1 controls fibroblast polarization and tissue fibrosis. Pharmacological and genetic inactivation of PU.1 disrupts the fibrotic network and enables reprogramming of fibrotic fibroblasts into resting fibroblasts, leading to regression of fibrosis in several organs. PubMed, Nature, 01/30/2019. (Also see Fibroblasts) This item was posted in the ISN Newsroom. Please check the newsroom daily for updates on scleroderma and other related articles.
  2. An orally–active adiponectin receptor agonist mitigates cutaneous fibrosis, inflammation and microvascular pathology in a murine model of systemic sclerosis (SSc). In vitro, AdipoRon abrogated profibrotic responses elicited by TGF-ß in normal fibroblasts, and reversed the inherently–activated profibrotic phenotype of SSc fibroblasts. PubMed, Sci Rep, 2018 Aug 7;8(1):11843. (Also see Fibroblasts) This item was posted in the ISN Newsroom. Please check the newsroom daily for updates on scleroderma and other related articles.
  3. Immune complexes (ICs) containing scleroderma (SSc)–specific autoantibodies induce a profibrotic and proinflammatory phenotype in skin fibroblasts. These data provide the first demonstration of the proinflammatory and profibrotic effects of SSc–ICs on fibroblasts, suggesting the potential pathogenicity of SSc autoantibodies. PubMed, Arthritis Res Ther, 2018 Aug 29;20(1):187. (Also see Fibroblasts and Antibodies in Systemic Scleroderma) This item was posted in the ISN Newsroom. Please check the newsroom daily for updates on scleroderma and other related articles.
  4. TLR4-dependent fibroblast activation drives persistent organ fibrosis in skin and lung. The results suggest that systemic scleroderma patients with high TLR4 activity might show optimal therapeutic response to selective inhibitors of MD2/TLR4 complex formation. PubMed, JCI Insight, 2018 Jul 12;3(13). (Also see Fibroblasts, Skin Fibrosis and Pulmonary Fibrosis Research) This item was posted in the ISN Newsroom. Please check the newsroom daily for updates on scleroderma and other related articles.
  5. Insights into myofibroblasts and their activation in scleroderma: opportunities for therapy? This review outlines the increasing complexity of the biological processes that leads to the appearance of the myofibroblast in normal functions and in diseased tissues. PubMed, Curr Opin Rheumatol, 07/31/2018. (Also see Fibroblasts) This item was posted in the ISN Newsroom. Please check the newsroom daily for updates on scleroderma and other related articles.
  6. Methyl-CpG-binding protein 2 (MeCP2) mediates antifibrotic effects in scleroderma (SSc) fibroblasts. This study demonstrates a novel role for MeCP2 in skin fibrosis and identifies MeCP2-regulated genes, which can be potentially targeted for therapy in SSc. PubMed, Ann rheumatologist Dis, 05/14/2018. (Also see Fibroblasts and Skin Fibrosis) This item was posted in the ISN Newsroom. Please check the newsroom daily for updates on scleroderma and other related articles.
  7. Pushing cells to self–destruct combats deadly fibrosis. New research offers clues for how to selectively destroy the cells known as myofibroblasts that drive the condition. Science Magazine, 12/13/2017. (Also see Fibroblasts) This item was posted in the ISN Newsroom. Please check the newsroom daily for updates on scleroderma and other related articles.
  8. The Antiretroviral nelfinavir mesylate (NFV), a potential therapy for systemic scleroderma. NFV abrogates TGF–ß1–mediated myofibroblast differentiation and pulmonary fibrosis through off–target protein binding and supports consideration of this FDA–approved medication as an anti–fibrotic agent. PubMed, Arthritis Rheumatol, 09/21/2017. (Also see Treatments for Pulmonary Fibrosis and Fibroblasts) This item was posted in the ISN Newsroom. Please check the newsroom daily for updates on scleroderma and other related articles.
  9. Downregulation of Aquaporin3 in Systemic Sclerosis (SSc) Dermal Fibroblasts. SSc manifestations like skin dryness, abnormal wound healing, and fibrotic lesions may be related to downregulation of AQP3 in SSc fibroblasts. PubMed, Iran J Allergy Asthma Immunol, 2017 Jun;16(3):228-234. (Also see Fibroblasts) This item was posted in the ISN Newsroom. Please check the newsroom daily for updates on scleroderma and other related articles.
  10. Unifying mechanism for different fibrotic diseases. Here, we demonstrate that many endstage fibrotic diseases converge in the activation of the Activator protein 1 transcription factor c-JUN in the pathologic fibroblasts. PubMed, Proc Natl Acad Sci U S A, 2017 May 2;114(18):4757-4762. (Also see Fibroblasts) This item was posted in the ISN Newsroom. Please check the newsroom daily for updates on scleroderma and other related articles.
  11. Innate Immunity in Systemic Sclerosis (SSc). Currently, no effective therapy exists and exploiting the innate immune system perturbation may be one possible avenue. Innate immune dysregulation is key in SSc pathogenesis and may represent a novel target. PubMed, Curr Rheumatol Rep, 2017 Jan;19(1):2. (Also see Fibroblasts) This item was posted in the ISN Newsroom. Please check the newsroom daily for updates on scleroderma and other related articles.
  12. Scleroderma (SSc) peripheral B lymphocytes secrete interleukin-6 and TGF–ß and activate fibroblasts. Peripheral B lymphocytes from SSc patients secreted IL-6 and TGF–ß, and activated fibroblasts in vitro. PubMed, Arthritis Rheumatol, 12/19/2016. (Also see Fibroblasts and Interleukins) This item was posted in the ISN Newsroom. Please check the newsroom daily for updates on scleroderma and other related articles.
  13. Bosentan and macitentan (ERA's) prevent the endothelial–to–mesenchymal transition (EndoMT) in systemic sclerosis: in vitro study. The present study provides further in vitro evidence of the use of ERA in inhibiting the EndoMT process, supporting the clinical efficacy of these drugs in SSc therapy and their usefulness for interfering with progressive fibrosis. PMC, Arthritis Res Ther, October 2016; 18: 228. (Also see Tracleer (Bosentan), Macitentan (Opsumit™) and Fibroblasts) This item was posted in the ISN Newsroom. Please check the newsroom daily for updates on scleroderma and other related articles.
  14. Transforming growth factor beta (TGF–beta1), int/Wingless (WNT) and sonic hedgehog (SHH) signaling in tumor progression and in fibrotic diseases. In this review, we focus on TGF–beta, WNT and SHH signal transduction pathways and describe small molecule inhibitors that are used in phase I/II clinical trials to treat fibrosis or fibrotic cancers. PubMed, Front Biosci (Schol Ed), 2017 Jan 1;9:31-45. (Also see Fibroblasts) This item was posted in the ISN Newsroom. Please check the newsroom daily for updates on scleroderma and other related articles.
  15. Mechanistic insight into the norepinephrine (NE)–induced fibrosis in systemic sclerosis (SSc). These results suggest that cold exposure and/or emotional stress–induced NE might contribute to the skin fibrosis via potentiation of IL-6 production from fibroblasts in SSc. PMC, Sci Rep, 2016; 6: 34012. (Also see Interleukins and Fibroblasts) This item was posted in the ISN Newsroom. Please check the newsroom daily for updates on scleroderma and other related articles.
  16. Toll–like receptor 9 (TLR9) signaling is augmented in systemic sclerosis (SSc) and elicits transforming growth factor–ß (TGF–ß)–dependent fibroblast activation. In patients with SSc, mitochondrialDNA and other damage–associated TLR9 ligands in the skin might trigger localized activation of TLR9 signaling, TGF–ß production and consequent fibroblast activation. PubMed, Arthritis Rheumatol, 03/04/2016. (Also see Causes of Scleroderma: Fibroblasts) This item was posted in the ISN Newsroom. Please check the newsroom daily for updates on scleroderma and other related articles.
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