细胞代谢在程序性细胞死亡的调控中。

Cell metabolism in the regulation of programmed cell death.

作者信息

Plas David R, Thompson Craig B

机构信息

Abramson Family Cancer Research Institute and Department Cancer Biology, University of Pennsylvania, Philadelphia, PA 19104, USA.

出版信息

Trends Endocrinol Metab. 2002 Mar;13(2):75-8. doi: 10.1016/s1043-2760(01)00528-8.

DOI:10.1016/s1043-2760(01)00528-8

PMID:11854022

Abstract

Increased cellular metabolism and resistance to apoptosis are two hallmarks of cell transformation. Recent progress in the understanding of the role of mitochondria in controlling apoptosis has brought attention to the links between elements of the apoptotic machinery and cellular metabolism. Here, we review the coordinated effects of growth factor withdrawal on bioenergetics and programmed cell death, and discuss the metabolic consequences of genes that prevent apoptosis, including the BCL2 family of genes and AKT.

摘要

细胞代谢增加和抗凋亡能力增强是细胞转化的两个标志。近年来，在理解线粒体在调控细胞凋亡中作用方面取得的进展，使人们开始关注凋亡机制各要素与细胞代谢之间的联系。在此，我们综述生长因子撤除对生物能量学和程序性细胞死亡的协同作用，并讨论包括BCL2基因家族和AKT在内的抗凋亡基因的代谢后果。