细胞凋亡
程序性细胞死亡
神经退行性变
Bcl-2家族
细胞生物学
平衡
疾病
生物
半胱氨酸蛋白酶
免疫学
癌症研究
医学
遗传学
内科学
作者
Rumani Singh,Anthony Letaï,Kristopher A. Sarosiek
标识
DOI:10.1038/s41580-018-0089-8
摘要
The loss of vital cells within healthy tissues contributes to the development, progression and treatment outcomes of many human disorders, including neurological and infectious diseases as well as environmental and medical toxicities. Conversely, the abnormal survival and accumulation of damaged or superfluous cells drive prominent human pathologies such as cancers and autoimmune diseases. Apoptosis is an evolutionarily conserved cell death pathway that is responsible for the programmed culling of cells during normal eukaryotic development and maintenance of organismal homeostasis. This pathway is controlled by the BCL-2 family of proteins, which contains both pro-apoptotic and pro-survival members that balance the decision between cellular life and death. Recent insights into the dynamic interactions between BCL-2 family proteins and how they control apoptotic cell death in healthy and diseased cells have uncovered novel opportunities for therapeutic intervention. Importantly, the development of both positive and negative small-molecule modulators of apoptosis is now enabling researchers to translate the discoveries that have been made in the laboratory into clinical practice to positively impact human health. BCL-2 family proteins are the mediators of apoptotic cell death. The balance between pro-apoptotic and pro-survival BCL-2 family members is differently regulated in various physiological contexts to modulate cellular apoptotic susceptibility. Perturbation of this balance causes excessive or insufficient cell death, leading to diseases such as neurodegeneration and cancer.
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