BCL-2, Apoptosis, Mitochondria, Neuronal Injury, Neuronal Development, Neurodegeneration, Ischemia, Excitotoxcity
This work was funded by Science Foundation Ireland (13/IA/1881 and 08/IN1/B1949) and the European Union FP7 Marie Curie IAPP program (OXY-SENSE; Contract 230641) to Jochen H.M. Prehn.
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 Ca(2+) homeostasis independent of their classical role in cell death signaling.
Physics | Physiology
Anilkumar U, Prehn JHM. Anti-apoptotic BCL-2 family proteins in acute neural injury. Frontiers in Cellular Neuroscience. 2014;8:281