Molecular pathogenesis of cigarette smoking-induced stable COPD
Molecular pathogenesis of cigarette smoking-induced stable COPD
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DOI：
10.1111/nyas.12619
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发表时间：
2015-01-01
期刊：
影响因子：
--
通讯作者：
Adcock, Ian
中科院分区：
文献类型：
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作者：
Caramori, Gaetano;Kirkham, Paul;Adcock, Ian
炎症是稳定型慢性阻塞性肺疾病（COPD）的核心特征，涉及气道和肺部结构细胞的激活以及浸润性炎症细胞的激活和/或募集。这导致许多促炎蛋白的表达增强，一些抗炎介质的表达减少。蛋白质表达的改变通常以细胞特异性的方式与基因表达谱的伴随变化相关。增加对转录因子的作用和导致其在稳定型COPD中激活的信号通路的了解，将为开发潜在的抗炎药物提供新的靶点。目前正在开发几种针对这些途径和/或转录因子的新化合物，用于治疗稳定期COPD。此外，临床使用的糖皮质激素药物通过其自身的转录因子糖皮质激素受体来控制炎症和抗炎基因的表达。
Inflammationis a central feature of stable chronic obstructive pulmonary disease( COPD) and involves both activation of structural cells of the airways and the lungs and the activation and/or recruitment of infiltrating inflammatory cells. This results in enhanced expression of many pro-inflammatory proteins and reduced expression of some anti-inflammatory mediators. An altered protein expression is generally associated with concomitant changes in gene expression profiles in a cell-specific manner. Increased understanding of the role of transcription factors and of the signaling pathways leading to their activation in stable COPD will provide new targets to enable the development of potential anti-inflammatory drugs. Several new compounds targeting these pathways and/or transcription factors are now in development for the treatment of stable COPD. Furthermore, glucocorticoids drugs already in clinical use act through their own transcription factor, the glucocorticoid receptor, to control the expression of inflammatory and anti-inflammatory genes.