期刊文献+

过氧化物酶体增殖物激活受体γ激动剂抗转化生长因子-β促器官纤维化作用的研究进展

Research Advancements of Peroxisome Proliferator-Activated Receptor γ Agonists Inhibiting Transforming Growth Factor-β-Induced Organ Fibrosis
原文传递
导出
摘要 目的总结过氧化物酶体增殖物激活受体γ(PPARγ)激动剂抗转化生长因子-β(TGF-β)促器官纤维化作用的研究进展。方法复习有关PPARγ激动剂抗TGF-β促器官纤维化作用的文献并进行综述。结果 TGF-β是一种主要的促纤维化细胞因子,能促进多种器官的纤维化进程,而PPARγ激动剂则可以有效地阻断TGF-β的信号传导,从而发挥抗器官纤维化的作用。结论研究PPARγ激动剂主要通过阻断TGF-β信号传导来实现抗器官纤维化的机理,有助于PPARγ激动剂在临床上的推广运用,为治疗器官纤维化疾病提供一种新途径。 Objective To summarize the research advancement of peroxisome proliferator-activated receptor γ(PPARγ) agonists inhibiting transforming growth factor-β(TGF-β)-induced organ fibrosis.Methods The related literatures on PPARγ agonists inhibiting TGF-β-induced organ fibrosis were reviewed.Results TGF-β was a major fibrosis-promoting cytokine,which could promote a variety of organ fibrosis.PPARγ agonists could effectively block TGF-β signal transduction,and then suppressed organ fibrosis well.Conclusions The main antifibrotic mechanism of PPARγ agonists is to inhibit TGF-β signal transduction.The studies on this mechanism will help promoting the clinical application of PPARγ agonists,and provide a new way of the treatment for organ fibrosis.
出处 《中国普外基础与临床杂志》 CAS 2011年第3期348-352,共5页 Chinese Journal of Bases and Clinics In General Surgery
关键词 过氧化物酶体增殖物激活受体Γ 转化生长因子-Β 纤维化 Peroxisome proliferator-activated receptor γ Transforming growth factor-β Fibrosis
  • 相关文献

参考文献2

二级参考文献75

  • 1Feng-guangYANG,Zhi-wenZHANG,Dian-qiXIN,Chang-jinSHI,Jie-pingWU,Ying-luGUO,You-feiGUAN.Peroxisome proliferator-activated receptor γ ligands induce cell cycle arrest and apoptosis in human renal carcinoma cell lines[J].Acta Pharmacologica Sinica,2005,26(6):753-761. 被引量:22
  • 2[1]Uitto J,Kouba D.Cytokine modulation of extracellular matrix gene expression:relevance to fibrotic skin diseases.J Dermatol Sci 2000; 24 Suppl 1:S60-S69
  • 3[2]Verrecchia F,Mauviel A.TGF-beta and TNF-alpha:antagonis tic cytokines controlling type I collagen gene expression.Cell Signal 2004; 16:873-880
  • 4[3]Verrecchia F,Mauviel A.Control of connective tissue gene expression by TGF beta:role of Smad proteins in fibrosis.Curr Rheumatol Rep 2002; 4:143-149
  • 5[4]Verrecchia F,Mauviel A.Transforming growth factor-beta signaling through the Smad pathway:role in extracellular matrix gene expression and regulation.J Invest Dermatol 2002; 118:211-215
  • 6[5]LeRoy EC,Trojanowska MI,Smith EA.Cytokines and human fibrosis.Eur Cytokine Netw 1990; 1:215-219
  • 7[6]Schiller M,Javelaud D,Mauviel A.TGF-beta-induced SMAD signaling and gene regulation:consequences for extracellular matrix remodeling and wound healing.J Dermatol Sri 2004; 35:83-92
  • 8[7]Grotendorst GR.Connective tissue growth factor:a mediator of TGF-beta action on fibroblasts.Cytokine Growth Factor Rev 1997; 8:171-179
  • 9[8]Leask A,Denton CP,Abraham DJ.Insights into the molecular mechanism of chronic fibrosis:the role of connective tissue growth factor in scleroderma.J Invest Dermatol 2004; 122:1-6
  • 10[9]Feng XH,Derynck R.Specificity and versatility in tgf-beta signaling through Smads.Annu Rev Cell Dev Biol 2005; 21:659-693

共引文献147

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部