Repair and Remodeling of airway epithelium after injury in Chronic Obstructive Pulmonary Disease.
Repair and Remodeling of airway epithelium after injury in Chronic Obstructive Pulmonary Disease.
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DOI：
10.1007/s13665-013-0052-2
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发表时间：
2013-09-01
期刊：
影响因子：
--
通讯作者：
Sajjan US
中科院分区：
文献类型：
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作者：
Ganesan S;Sajjan US
慢性阻塞性肺病被认为是由于长期接触香烟烟雾、职业或其他环境危害而产生的，它包括气道和实质。细菌在气道的急性感染或慢性定植也可能导致 COPD 肺部疾病的发生和/或进展。气道上皮是吸入环境因素和病原体的主要目标。长期暴露于环境因素导致的重复性损伤可能导致气道上皮修复相关途径持续激活，例如上皮间质转化、祖细胞迁移和增殖改变以及导致气道重塑的异常再分化。需要开发模拟 COPD 中观察到的慢性气道疾病的模型系统，以了解 COPD 特有的异常气道上皮修复的分子机制，并开发专注于气道上皮修复的新疗法。
COPD is thought to develop as a result of chronic exposure to cigarette smoke, occupational or other environmental hazards and it comprises both airways and parenchyma. Acute infections or chronic colonization of airways with bacteria may also contribute to development and/or progression of COPD lung disease. Airway epithelium is the primary target for the inhaled environmental factors and pathogens. The repetitive injury as a result of chronic exposure to environmental factors may result in persistent activation of pathways involved in airway epithelial repair, such as epithelial to mesenchymal transition, altered migration and proliferation of progenitor cells, and abnormal redifferentiation leading to airway remodeling. Development of model systems which mimics chronic airways disease as observed in COPD is required to understand the molecular mechanisms underlying the abnormal airway epithelial repair that are specific to COPD and to also develop novel therapies focused on airway epithelial repair.