慢性阻塞性肺疾病气道上皮损伤后的修复和重塑。

Shyamala Ganesan, Uma S Sajjan
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引用次数: 53

摘要

慢性阻塞性肺病被认为是由于长期暴露于香烟烟雾、职业或其他环境危害而发展起来的,它包括气道和实质。急性感染或气道细菌的慢性定植也可能导致慢性阻塞性肺病的发生和/或进展。气道上皮是吸入环境因素和病原体的首要目标。慢性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通路的持续激活,如上皮向间充质转化、祖细胞迁移和增殖的改变以及导致气道重塑的异常再分化。开发模拟COPD中观察到的慢性气道疾病的模型系统,需要了解COPD特异性气道上皮异常修复的分子机制,也需要开发专注于气道上皮修复的新疗法。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Repair and Remodeling of airway epithelium after injury in Chronic Obstructive Pulmonary Disease.

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.

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