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Found 19 results

  1. Kelch-like protein 42 is a pro-fibrotic ubiquitin E3 ligase involved in in systemic sclerosis (SSc). Our findings indicate that the KLHL42-PPP2R5e axis controls pro-fibrotic signaling in SSc lung fibroblasts. PubMed, J Biol Chem, 02/17/2020. (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. Long non-coding RNA HOTAIR drives EZH2-dependent myofibroblast activation in systemic sclerosis through miRNA 34a-dependent activation of NOTCH. Our data indicate that the EZH2-dependent epigenetic phenotype of myofibroblasts is driven by HOTAIR. PubMed, Ann rheumatologist Dis, 02/10/2020. (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. Dipeptidylpeptidase 4 as a Marker of Activated Fibroblasts and a Potential Target for the Treatment of Fibrosis in Systemic Sclerosis (SSc). DPP-4 characterizes a population of activated fibroblasts and shows that DPP-4 regulates TGFβ-induced fibroblast activation in the fibrotic skin of SSc patients. PubMed, Arthritis Rheumatol, 2020 Jan;72(1):137-149. (Also see Fibroblasts) This item was posted in the ISN Newsroom. Please check the newsroom daily for updates on scleroderma and other related articles.
  4. Antibodies against specific extractable nuclear antigens (ENAs) as diagnostic and prognostic tools and inducers of a profibrotic phenotype in cultured human skin fibroblasts: are they functional? This study suggests a pathogenic role of scleroderma-specific autoantibodies to directly induce pro-fibrotic activation in human dermal fibroblasts. PubMed, Arthritis Res Ther, 2019 Jun 24;21(1):152. (Also see Fibroblasts and Antibodies) This item was posted in the ISN Newsroom. Please check the newsroom daily for updates on scleroderma and other related articles.
  5. Targeting of dermal myofibroblasts through death receptor 5 arrests fibrosis in mouse models of scleroderma. In vivo, TLY012 reverses established skin fibrosis to near–normal skin architecture in mouse models of scleroderma. PubMed, Nat Commun, 2019 Mar 8;10(1):1128. (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. Evolving insights into the cellular and molecular pathogenesis of fibrosis in systemic sclerosis (SSc). After reviewing the major and emerging cellular and molecular mechanisms underlying SSc, this article looks to identify clinical applications where this new molecular knowledge may allow for targeted treatment and personalized medicine approaches. PubMed, Transl Res, 02/23/2019. (Also see Fibroblasts) This item was posted in the ISN Newsroom. Please check the newsroom daily for updates on scleroderma and other related articles.
  7. Identification of regulators of the myofibroblast phenotype of primary dermal fibroblasts from early diffuse systemic sclerosis (dSSc) patients. Our results demonstrated the value of carefully–phenotyped SSc dermal fibroblasts as a platform for SSc target and drug discovery. PubMed, Sci Rep, 2019 Mar 14;9(1):4521. (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. 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.
  9. 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.
  10. 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.
  11. 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.
  12. 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.
  13. 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.
  14. 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.
  15. 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.
  16. 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.
  17. 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.
  18. 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.
  19. 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.
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