期刊
COPD-JOURNAL OF CHRONIC OBSTRUCTIVE PULMONARY DISEASE
卷 6, 期 3, 页码 201-210出版社
TAYLOR & FRANCIS INC
DOI: 10.1080/15412550902905953
关键词
Apoptosis; repair; fibroblast; myofibroblast; extracellular matrix; TGF-beta 1; Chronic Obstructive Pulmonary Disease: A Global Health Crisis
资金
- NHLBI NIH HHS [K08 HL081059, R01 HL067967, R01 HL67967] Funding Source: Medline
Emphysema is characterized by the destruction of alveolar parenchymal tissue and the concordant loss of lung epithelial cells, endothelial cells, and interstitial mesenchymal cells. Key features in the pathobiology of emphysema include inflammation, alveolar epithelial cell injury/apoptosis, and excessive activation of extracellular matrix (ECM) proteases. Mesenchymal cells are versatile connective tissue cells that are critical effectors of wound-repair. The excessive loss of connective tissue and the destruction of alveolar septae in emphysema suggest that the mesenchymal cell reparative response to epithelial injury is impaired. Yet, the mechanisms regulating mesenchymal cell (dys)function in emphysema remain poorly understood. We propose that mesenchymal cell fate, modulated by transforming growth factor beta-1 (TGF-beta 1) and the balance of ECM proteases and antiproteases, is a critical determinant of the emphysema phenotype. We examine emphysema in the context of wound-repair responses, with a focus on the regulation of mesenchymal cell fate and phenotype. We discuss the emerging evidence supporting that genetic factors, inflammation and environmental factors, including cigarette smoke itself, collectively impair mesenchymal cell survival and function, thus contributing to the pathogenesis of emphysema.
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