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


METHODS
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", PD", "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.
Department of Respiratory Medicine, The Second Xiangya Hospital, Central South University, Changsha, Hunan, China.
Huihui
H
Zeng
Xianglong
X
Kong
Hong
H
Peng
Yan
Y
Chen
Shan
S
Cai
Hong
H
Luo
Ping
P
Chen
D000818:Animals; D017209:Apoptosis; D004195:Disease Models, Animal; D006801:Humans; D008168:Lung / Q000473:pathology; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000502:physiology*; D029424:Pulmonary Disease, Chronic Obstructive / Q000209:etiology / Q000473:pathology* / Q000628:therapy
D019253:Proto-Oncogene Proteins c-bcl-2