Department of Respiratory Medicine, The Second Xiangya Hospital, Central South University, Changsha, Hunan, China.
Eur Rev Med Pharmacol Sci. 2012 Jun;16(6):711-27.
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.
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.
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.
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.
慢性阻塞性肺疾病（COPD）的特征是气道和肺气肿的慢性炎症、肺实质和肺泡结构的进行性破坏。在 COPD 中已经观察到肺或肺外细胞的凋亡，并且已经表明它有助于 COPD 的起始和进展。凋亡与其他机制（如炎症、蛋白水解/抗蛋白水解失衡、氧化应激等）的相互作用也在 COPD 发病机制中得到了描述。Bcl-2 家族蛋白通过维持线粒体来调节凋亡。这些蛋白由抗凋亡和促凋亡成员组成，它们之间的相互作用决定了线粒体是否应该通过释放促凋亡因子来启动程序性死亡。已经报道抗凋亡蛋白对 COPD 具有保护潜力，而促凋亡蛋白则被描述为有助于 COPD。
本综述强调了凋亡的参与，特别是与 Bcl-2 家族蛋白失调相关的凋亡在 COPD 中的作用。我们通过 Pubmed 引擎搜索了“凋亡”、“PD”、“Bcl-2”、“香烟烟雾”和“肺泡细胞”等关键词。
凋亡过程已经取得了很大的进展。然而，关于导致肺泡破坏的这一特定过程，仍然存在相当大的知识差距。启动和进展凋亡的主要因素是 Bcl-2 家族成员。
更好地了解肺组织和细胞中的凋亡过程和 Bcl-2 家族成员显然很重要，因为它可能导致为 COPD 确定新的治疗策略。
