期刊
CURRENT PULMONOLOGY REPORTS
卷 2, 期 3, 页码 145-154出版社
SPRINGER
DOI: 10.1007/s13665-013-0052-2
关键词
Barrier function; Mucociliary clearance; Innate immunity; Asthma; EMT; Airway progenitor cells; Cigarette smoke; Respiratory infection; EGFR; Mucus metaplasia; Mucus hyperplasia
资金
- National Institute of Health [HL089772, AT004793]
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 that mimic 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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