文章发表！CTRP3

来自 : 发布时间：2025-03-31

文章发表！CTRP3 [Journal of Molecular Medicine] [文章一]美国Aviscera产品, Aviscera Bioscience CTRP3蛋白和试剂盒(Aviscera Bioscience, Inc. Santa Clara, CA).助力科学家发表文章CTRP3 attenuates post-infarct cardiac fibrosis by targeting Smad3 activation and inhibiting myofibroblast differentiation 到SCI检索期刊Journal of Molecular Medicine影响因子5.1Original ArticleJournal of Molecular MedicineFirst online: 03 July 2015AbstractC1q/tumor necrosis factor-related protein-3 (CTRP3) is a novel adipokine with modulation effects on metabolism, inflammation, and cardiovascular system. This study aimed to investigate the effect of CTRP3 on cardiac fibrosis and its underlying mechanism. The myocardial expression of CTRP3 was significantly decreased after myocardial infarction (MI). Adenovirus-delivered CTRP3 supplement attenuated myocardial hypertrophy, improved cardiac function, inhibited interstitial fibrosis, and decreased the number of myofibroblasts post-MI. In cultured adult rat cardiac fibroblasts (CFs), CTRP3 attenuated cell proliferation; migration; and the expression of connective tissue growth factor, collagen I, and collagen III induced by transforming growth factor (TGF)-β1. Moreover, CTRP3 inhibited whereas CTRP3 small interfering RNA (siRNA) facilitated the expression of α-SMA and profibrotic molecules induced by TGF-β1. CTRP3 also attenuated TGF-β1-induced Smad3 phosphorylation, nuclear translocation, and interaction with p300. CTRP3 increased the phosphorylation of AMP-activated protein kinase (AMPK) and Akt in both rat hearts and CFs. Adenine 9-β-d-arabinofuranoside (AraA), an AMPK inhibitor, abolished the protective effect of CTRP3 against TGF-β1-induced profibrotic response and Smad3 activation. Taken together, CTRP3 attenuates cardiac fibrosis by inhibiting myofibroblast differentiation and the subsequent extracellular matrix production. AMPK is required for the anti-fibrotic effect of CTRP3 through targeting Smad3 activation and inhibiting myofibroblast differentiation.Key message·         CTRP3 alleviates cardiac fibrosis in a rat post-MI model and in cardiac fibroblasts.·         CTRP3 inhibits fibroblast-to-myofibroblast differentiation.·         CTRP3 exerts anti-fibrotic effect through targeting Smad3 activation.·         AMPK mediates the anti-fibrotic effect of CTRP3 by inhibition of Smad3 activation.KeywordsC1q/tumor necrosis factor-related protein-3 (CTRP3) Myocardial infarction (MI) Cardiac fibrosis Myofibroblast differentiation Smad3 为了方便广大科研工作者，我公司代理美国AVISCERA Bioscience品牌CTRP3蛋白和试剂盒相关产品。欢迎大家寻购。联系电话010-61734358。[文章二]美国Aviscera产品, Aviscera Bioscience CTRP3蛋白和试剂盒(Aviscera Bioscience, Inc. Santa Clara, CA).助力科学家发表文章Overexpression of C1q/Tumor Necrosis Factor–Related Protein-3 Promotes Phosphate-Induced Vascular Smooth Muscle Cell Calcification Both In Vivo and In Vitro

•  到SCI检索期刊Vascular Biology

影响因子6.5[文章三]文章发表！CTRP3试剂盒 AVISCERA BIOSCIENCE  CTRP3Elisa kit产品助力科学家发表文章Serum C1q/TNF-related protein-3 (CTRP3) levels are decreased in obesity and hypertension and are negatively correlated with parameters of insulin resistance 到SCI检索期刊Diabetology & Metabolic Syndrome IMPACT FACTOR 2.17文章链接地址：http://www.dmsjournal.com/content/7/1/33  为了方便广大科研工作者，我公司代理美国AVISCERA Bioscience品牌的人CTRP家族的蛋白及试剂盒。欢迎大家寻购。联系电话010-61734358。   动脉粥样硬化的相关分子标志物：Cd44/ CD44 antigenCtgf/  Connective tissue growth factorCxcll/ Chemokine (C-X-C motif) ligand 1Fgf2/  Fibroblast growth factor 2Il--1a/ Interleukin 1 alphaIl-lb/  Interleukin 1 betaIl-2/    Interleukin 2Il-3/    Interleukin 3Il-4/    Interleukin 4Il-5/    Interleukin 5Lif/    Leukemia inhibitory factorLyplal/     Lysophospholipase 1 溶血磷脂酶1LP-PLA2   lipoprotein-associated phospholipase A2  脂蛋白相关性磷脂酶A2Mmp3/    Matrix metallopeptidase 3

Monocyte Chemoattractant Protein 1 (MCP-1)PTX3  pentraxin-3  正五聚体蛋白-3

Tgfbl/ Transforming growth factor, beta 1Tnc/   Tenascin CTnf/   Tumor necrosis factorVcaml/     Vascular cell adhesion molecule 1