Anti-apoptotic BCL-2 family proteins in acute neural injury

被引：78

作者：

Anilkumar, Ujval ^{[1
]}

Prehn, Jochen H. M. ^{[1
]}

机构：

[1] Royal Coll Surgeons Ireland, Dept Physiol & Med Phys, Ctr Study Neurol Disorders, Dublin 2, Ireland

来源：

FRONTIERS IN CELLULAR NEUROSCIENCE | 2014年 / 8卷

基金：

爱尔兰科学基金会;

关键词：

BCL-2; apoptosis; mitochondria; neuronal injury; neuronal development; neurodegeneration; ischemia; excitotoxcity; PROGRAMMED CELL-DEATH; OUTER-MEMBRANE PERMEABILIZATION; ISCHEMIC BRAIN-INJURY; SPINAL-CORD-INJURY; X MESSENGER-RNA; OXIDATIVE STRESS; BH3-ONLY PROTEINS; NEURONAL APOPTOSIS; NERVOUS-SYSTEM; NEURODEGENERATIVE DISORDERS;

D O I：

10.3389/fncel.2014.00281

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

Cells under stress activate cell survival and cell death signaling pathways. Cell death signaling frequently converges on mitochondria, a process that is controlled by the activities of pro- and anti-apoptotic B-cell lymphoma 2 (BCL-2) proteins. In this review, we summarize current knowledge on the control of neuronal survival, development and injury by anti-apoptotic BCL-2 family proteins. We discuss overlapping and differential effects of the individual family members BCL-2, BCL-extra long (BCL-XL), myeloid cell leukemia 1 (MCL-1), and BCL2-like 2 (BCL-W) in the control of survival during development and pathophysiological processes such as trophic factor withdrawal, ischemic injury, excitotoxicity, oxidative stress and energy stress. Finally we discuss recent evidence that several anti-apoptotic BCL-2 proteins influence mitochondrial bioenergetics and control neuronal Ca2+ homeostasis independent of their classical role in cell death signaling.

引用

页数：6

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