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组蛋白去乙酰化酶2与慢性阻塞性肺疾病 被引量:6

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摘要 慢性阻塞性肺疾病(简称慢阻肺)目前居全球死亡原因的第4位,慢阻肺的发病机制与呼吸道及肺部对香烟烟雾、生物燃料等慢性刺激物的炎症反应有关[1]。慢阻肺的气道和肺部炎症持续存在,这与多种炎性基因的过度表达有关[2]。炎性基因的表达由DNA周围核心组蛋白的乙酰化和去乙酰化所调节,目前研究表明组蛋白去乙酰化酶2(histone deacetylase 2,HDAC2)的降低参与了慢阻肺的发病过程,并且与糖皮质激素抵抗有关[3-6]。
出处 《中国呼吸与危重监护杂志》 CAS 北大核心 2015年第4期410-413,共4页 Chinese Journal of Respiratory and Critical Care Medicine
基金 首都医学发展科研基金(编号:2011-2002-03)
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同被引文献56

  • 1李晓丹,王强.补肺颗粒通过调控Akt通路对慢阻肺大鼠肺组织自噬和凋亡的影响[J].武汉大学学报(医学版),2020,41(6):904-910. 被引量:11
  • 2慢性阻塞性肺疾病诊治指南(2013年修订版)[J].中国医学前沿杂志(电子版),2014,6(2):67-80. 被引量:2039
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  • 5Malhotra D, Thimmulappa RK, Mereado N, et al. Denitrosylation of HDAC2 by targeting Nrf2 restores glucocorticosterold sensitivity in macrophages from COPD patients[ J]. J Clin Invest, 2011,121 ( 11 ) :4289-4302.
  • 6Khorasani N, Baker J, Johnson M, et al. Reversal of corticosteroid insensitivity by p38 MAPK inhibition in peripheral blood mononu- clear cells from COPD [ J ]. Int J Chron Obstruct Pulmon Dis, 2015,10:283-291.
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