Apoptosis and Bcl-2 family proteins, taken to chronic obstructive pulmonary disease

H.-H. Zeng, X.-L. Kong, H. Peng, Y. Chen, S. Cai, H. Luo, P. Chen

Department of Respiratory Medicine, The Second Xiangya Hospital, Central South University, Changsha, Hunan (China)

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• Respiratory Medicine

BACKGROUND: Chronic obstructive pulmonary disease (COPD) is characterized by chronic inflammation of airway and emphysema, progressive destruction of lung parenchyma and alveolar structure. Apoptosis of pulmonary or extrapulmonary cells has been observed in COPD and has been shown to contribute to the initiation and progression of COPD. The interactions of apoptosis and other mechanisms, such as inflammation, proteolytic/antiproteolytic imbalance, oxidative stress and so on, also have been described in COPD pathogenesis. The Bcl-2 family proteins regulate apoptosis via mitochondrial maintenance. These proteins consist of anti- and pro-apoptotic members, and interactions of them decide whether the mitochondria should initiate the programmed death by releasing pro-apoptotic factors. The anti-apoptotic proteins have been reported to present protective potential for COPD, whereas the pro-apoptotic proteins have been described to contribute to COPD.

DESIGN: This review highlights the participation of apoptosis, particularly those related to deregulation of Bcl-2 family proteins in COPD. We searched key words, such as “apoptosis”, “COPD”, “Bcl-2”, “cigarette smoke” and “alveolar cells”, by Pubmed engine.

RESULTS: There has been a strong progress in apoptotic processes. However, there are still considerable gaps in knowledge regarding this specific process causing alveolar destruction. The major contributing factors to the initiation and progressing of apoptosis are Bcl-2 family members.

CONCLUSIONS: Better understanding of apoptotic process and Bcl-2 family members in the lung tissue and cells is apparently important, as it may lead to the identification of novel therapeutic strategies for COPD.

Corresponding Author: Ping Chen, MD; e-mail: pingchen0731@sina.com

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