摘要
目前已经发现的BCL-2蛋白家族按功能可分为2类，一类具有抑制凋亡作用（如BCL-2），而另一类具有促进凋亡作用（如Bax）。BCL-2家族调节细胞凋亡机制目前仍不清楚，大多认为与BCL-2调节细胞的氧化应激及调节钙离子的跨膜运动有关。近几年研究证明，BCL-2家族蛋白主要直接控制线粒体外膜通透性的改变而引起细胞凋亡，除此之外，尚存在BCL-2不敏感的凋亡途径；细胞凋亡在肺纤维化中发挥重要的作用，包括上皮细胞的凋亡过度和成纤维细胞的凋亡不足；BCL-2家族篮㈠在肺纤维化中发挥着启动和调节线粒体途径引起的细胞凋亡开关作用。
BCL-2 family proves to be composed of proapoptotic and antiapoptotie proteins up to now. Antiapoptotic members,such as BCL-2, promote cell survival by inhibiting the function of the proapoptotic BCL-2 proteins such as Bax. Exact mechanism by which BCL-2 family proteins regulates apoptosis is still unclear,but at least three different models of regulation have emerged from the literature. Since the BCL-2 family proteins have the potential to affect multiple mechanisms of apoptosis including calcium dysregulation, and oxidative stess, BCL-2 family members are important regulators of the mitochondrial pathway of apoptosis. These proteins decide whether the mitochondria should initiate the cell death program and release proapoptotic factors such as cytochrome C. It is important for apoptosis to induce pulmonary fibrosis including apoptosis susceptibility in epithelial cells and apoptosis resistance in myofibroblasts. BCL-2 proteins play a key role in regulating apoptosis in the pulmonary fibrosis. This review summarizes the current understanding on role of BCL-2 proteins in the pulmonary fibrosis.
出处
《国际呼吸杂志》
2008年第24期1500-1504,共5页
International Journal of Respiration
基金
湖南省教育厅基金资助项目（08C734）
