Wu Hai-Jian, Pu Jia-Li, Krafft Paul R, Zhang Jian-Min, Chen Sheng
Department of Neurosurgery, Second Affiliated Hospital, School of Medicine, Zhejiang University, 88 Jiefang Road, Hangzhou, 310009, Zhejiang, China.
Cell Mol Neurobiol. 2015 Jan;35(1):85-99. doi: 10.1007/s10571-014-0116-z. Epub 2014 Sep 26.
Autophagy involves degradation of dysfunctional cellular components through the actions of lysosomes. Apoptosis is the process of programmed cell death involving a series of characteristic cell changes. Autophagy and apoptosis, as self-destructive processes, play an important role in the pathogenesis of neurological diseases; and a crosstalk between "self-eating" (autophagy) and "self-killing" (apoptosis) plays an important role in pathological cellular adaptation. Expert knowledge of autophagy and apoptosis has increased in recent years, particularly in regards to cellular and molecular mechanisms. The crosstalk between autophagy and apoptosis was partially uncovered and several key molecules, including Bcl-2 family members, Beclin 1, and p53 were identified. However, the precise mechanisms of such a crosstalk remain to be elucidated. This current review article aims to summarize key mediators of the autophagy-apoptosis crosstalk in pathological conditions, and to highlight recent advances in the field, as well as to discuss further investigations and therapeutic potentials of manipulating those mechanisms in central nervous system diseases.
自噬涉及通过溶酶体的作用降解功能失调的细胞成分。凋亡是程序性细胞死亡的过程，涉及一系列特征性的细胞变化。自噬和凋亡作为自我破坏过程，在神经疾病的发病机制中起重要作用；“自噬”（自噬）和“自杀”（凋亡）之间的相互作用在病理性细胞适应中起重要作用。近年来，关于自噬和凋亡的专业知识有所增加，特别是在细胞和分子机制方面。自噬和凋亡之间的相互作用已部分被揭示，并且鉴定了几个关键分子，包括Bcl-2家族成员、Beclin 1和p53。然而，这种相互作用的确切机制仍有待阐明。这篇综述文章旨在总结病理条件下自噬-凋亡相互作用的关键介质，突出该领域的最新进展，并讨论在中枢神经系统疾病中操纵这些机制的进一步研究和治疗潜力。
