期刊文献+

组蛋白脱乙酰化酶抑制剂抗心脏纤维化作用及免疫机制 被引量:2

Anti-cardiac fibrosis effect and immunologic mechanism of histone deacetylases inhibitors
原文传递
导出
摘要 可逆性组蛋白乙酰化在调节心肌纤维化过程中具有核心作用,而组蛋白乙酰基转移酶(HATs)和组蛋白脱乙酰化酶(HDACs)是决定组蛋白乙酰化程度的两种主要酶。组蛋白脱乙酰酶抑制剂(HDACIs)具有抗纤维化作用,可减少心脏细胞凋亡、肥大以及心室纤维化,其抗心脏纤维化作用与其对心脏成纤维细胞、肾素一血管紧张素一醛固酮系统及其免疫机制密切相关。不久的未来,HDAC抑制剂可能作为一种新型的治疗心衰的药物。 The reversible histone acetylation plays a crucial role in regulating myocardial fibrosis. His- tone acetyl transferase (HATs) and histone acetylation enzyme (HDACs) are two key enzymes which determine the leve| of histone acetylation. Histone deacetylases inhibitors, HDACIs show anti-cardiac fibrosis effect due to their inhibition on cardiac fibroblasts or renin-angiotensin-aldosterone system. HDACIs can reduce myocardial apoptosis, myocardial hypertrophy and myocardial fibrosis. In the future, HDAC inhibitor may be employed as a novel drug in the treatment of heart failure.
出处 《国际免疫学杂志》 CAS 2015年第4期371-374,共4页 International Journal of Immunology
基金 国家自然科学基金面上项目(81270310) 黑龙江省科技攻关项目(GC06C41902) 黑龙江省教育厅海外学人重点项目(1252H0013) 黑龙江省留学归国基金 哈医大于维汉青年基金
关键词 组蛋白脱乙酰化酶 组蛋白脱乙酰化酶抑制剂 心脏纤维化 Histone acetylation enzyme Histone deacetylases inhibitors Cardiac fibrosis
  • 相关文献

参考文献22

  • 1Gong F, Miller KM. Mammalian DNA repair: HATs and HDACs make their mark through histone aeetylation [ J ] ~ Murat Res, 2013,750(1-2) :23-30.
  • 2Stafford JM, Raybuck JD, Ryabinin AE, et al. Increasing histone acetylatian it~ the hippocampus-infralimbic network enhances fear extinction [ J ]. Biol Psychiatry ,2012,72 ( 1 ) :25-33.
  • 3Deubzer HE,Schier MC, Oehme I, et al. HDACI 1 is a novel drug target in carcinomas [ J ]. Int J Cancer,2013,132 (9) :2200-2208.
  • 4彭昌,田杰.组蛋白乙酰化酶和去乙酰化酶对心脏发育影响的研究进展[J].广东医学,2013,34(24):3818-3820. 被引量:3
  • 5Dent P. HDACIs and the inhibition of invasive potential[ J]. Canc- er Biol Ther,2013,14 ( 9 ) :776-777.
  • 6郭艳琳,康玉明,杨志明,王淑秋,秦达念.组蛋白脱乙酰化酶抑制剂对炎性细胞因子表达的影响[J].中国药物与临床,2010,10(4):365-368. 被引量:5
  • 7Wong A, Young B. The Future is Now: Frontiers on Display at Yale-NAVBO Cardiovascular Inflammation and Remodeling Sym- posium[ J]. Yale J Biol Med ,2014,87 (4) :593-599.
  • 8McKinsey TA. Targeting Inflammation in Heart Failure with Histone Deacetylase Inhibitors [ J ]. Mol Med,2011,17 (5-6) :434-441.
  • 9Nural-Guvener HF,Zakharova L,Nimlos J,et al. HDAC class I in-hihitor, Mocetinostat, reverses cardiac fiborsis in heart failure and diminishes CD90 + cardiac myofibmblast activation [ J]. Fibrogen- esis Tissue Repair,2014,7 (2) : 10.
  • 10Chen W, Frangogiannis NG. Fibroblasts in post-infarction inflam- mation and cardiac repair[ J]. Biochim Biophys Acta,2013,1833 (4) :945-953.

二级参考文献51

  • 1Adcock IM,Ford P,Ito K,et al.Epigenetics and airways disease.Respir Res,2006,7(1):21.
  • 2Xu WS,Parmigiani RB,Marks PA.Histone deacetylase inhibitors:molecular mechanism of action.Oncogene,2007,26(37):5541-5552.
  • 3Hayden MS,Ghosh S.Signaling to NF-κB.Genes Dev,2004,18(18):2195-2224.
  • 4Dong J,Jimi E,Zhong H,et al.Repression of gene expression by unphosphorylated NF-kappaB p65 through epigenetic mechanisms.Genes Dev,2008,22(9):1159-1173.
  • 5Chen LF,Williams SA,Mu Y,et al.NF-kappaB RelA phosphorylation regulates RelA acetylation.Mol Cell Biol,2005,25(18):7966-7975.
  • 6Chen LF,Fischle W,Verdin E,et al.Duration of nuclear NF-κB action regulated by reversible acetylation.Science,2001,293(31):1653-1657.
  • 7Kiernan R,Brès V,Ng RW,et al.Post-activation turn-off of NF-κB-dependent transcription is regulated by acetylation of p65.J Biol Chem,2003,278(4):2758-2766.
  • 8Hu J,Colburn NH.Histone deacetylase inhibition down-regulates cyclin D1 transcription by inhibiting nuclear factor-κB/p65 DNA binding.Mol Cancer Res,2005,3(2):100-109.
  • 9Dokmanovic M,Clarke C,Marks PA.Histone deacetylase inhibitors:overview and perspectives.Mol Cancer Res,2007,5(10):981-989.
  • 10Adcock IM.HDAC inhibitors as anti-inflammatory agents.Br J Pharmacol,2007,150(7):829-831.

共引文献9

同被引文献10

引证文献2

二级引证文献3

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