细胞凋亡分子机制的研究进展

ADVANCES ON RESEARCH OF MOLECULAR MECHANISMS IN APOPTOSIS

细胞凋亡(apoptosis),又称程序性细胞死亡(programmed cell death),是一种进化保守和遗传决定的细胞自杀,其性质为生理性。在多细胞动物,凋亡对正常机体的发育和自身稳定起着极其重要的作用。现已发现,有许多疾病的发生和发展与凋亡机制异常有关。细胞凋亡为生物医学领域中最热门的课题之一。在过去5年里对细胞凋亡的分子机制的研究取得了突破性进展。现已证明,多种基因产物参与了细胞凋亡过程,其中包括肿瘤坏死因子受体(TNFR)基因超家族的产物死亡受体(death receptors)、连接蛋白(adapters)、天门冬氨酸特异性半胱氨酸蛋白酶(caspases)和Bcl-2家族调节蛋白(Bcl-2 protein family regulators)等。目前对每组蛋白的成员的化学特性、基本功能和它们的上游和下游的相互作用分子等均有了较清楚的了解。这些结果为发展以凋亡机制相关蛋白为靶分子的治疗性细胞凋亡干预手段奠定了基础。

Apoptosis, also known as programmed cell death, is an evolutionarily conserved and genetically controlled cell suicide. Apoptosis plays important roles both in development and in homeostasis of metazoans, and it was attracted great interests from researches. Many diseases have heen found related to the defect of apoptotic programs. A breakthrough has been made in understanding of molecular mechanisms of apoptosis during the past 5 years. It has been found that several groups of gene products are involved in apoptotic mechanisms, including death receptors belonging to TNFR gene super-family , caspases and Bcl-2 protein family regulators. The biochemical characteristics and basic function of the members of each group of proteins as well as their upstream and downstream interactive proteins have been defined clearly. All the findings will form the basis for developing therapeutic intervention of apoptosis targeting to the composed proteins of apopotic pathways.