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ADAM家族金属蛋白酶在调控肺部炎症中的作用 被引量:2

Role of ADAM family metalloproteinases in the regulation of lung inflammation
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摘要 急性和慢性的肺部炎症是被几种内源性的介质驱动和控制的,而这些介质通过一个解聚素及金属蛋白酶(ADAM)家族成员经历了从表面表达蛋白到溶解蛋白形态的蛋白水解转换。TNF及表皮生长因子受体配体正好是许多作用底物中的一类,通过这些作用底物蛋白酶可调节肺部的炎症及生长过程。ADAM10及ADAM17是这种蛋白酶家族中最重要的成员,在大多数肺细胞中有构成性表达。近期研究显示,它们是调节肺部急性炎症的最重要的脱落酶。ADAM17促进内皮细胞和上皮细胞的渗透性,跨内皮的白细胞迁移及炎症介质的产生。ADAM10对白细胞迁移及中性粒细胞在肺部聚集是十分关键的。总之,既往研究已证实ADAM家族酶可抑制肺部的急性炎症反应过程,而这些有潜力的结果可鼓励进一步研究基于选择ADAMs的靶向治疗策略。 Acute and chronic lung inflammation is driven and controlled by several endogenous mediators that undergo proteolytic conversion from surface-expressed proteins to soluble variants by a disintegrin and metalloproteinase( ADAM)-family members. TNF and epidermal growth factor receptor ligands are just some of the many substrates by which these proteases regulate inflammatory or regenerative processes in the lung. ADAM10 and ADAM17 are the most prominent members of this protease family. They are constitutively expressed in most lung cells and,as recent researches have shown,are the pivotal shedding enzymes mediating acute lung inflammation. ADAM17 promotes endothelial and epithelial permeability,transendothelial leukocyte migration, and inflammatory mediator production. ADAM10 is critical for leukocyte migration and alveolar leukocyte recruitment. In conclusion,previous studies have confirmed that ADAM-family members suppress acute inflammatory responses in the lung,and these promising results encourage further researches to develop therapeutic strategies based on selected ADAMs.
作者 钟荣 肖军
出处 《华夏医学》 CAS 2017年第4期133-137,共5页 Acta Medicinae Sinica
基金 广西壮族自治区卫生厅自筹经费项目资助(Z2014323) 广西壮族自治区临床重点专科建设项目资助[桂卫(2014)13]
关键词 解聚素及金属蛋白酶 肺部炎症 蛋白水解 ADAM lung inflammation proteolysis
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