- 作者: Ruiqiao Guan, Wei Zou, Xiaohong Dai, Xueping Yu, Hao Liu, Qiuxin Chen and Wei Teng
- 作者服務機構: 1. Heilongjiang University Of Chinese Medicine, Harbin 150040, Heilongjiang province, China 2. First Affiliated Hospital of Heilongjiang University Of Chinese Medicine, Harbin 150040, Heilongjiang province, China
- 中文摘要:
- 英文摘要:
Mitochondria autophagy, termed as mitophagy, is a mechanism of specific autophagic elimination of mitochondria. Mitophagy controls the quality and the number of mitochondria, eliminating dysfunctional or excessive mitochondria that can generate reactive oxygen species (ROS) and cause cell death. Mitochondria are centrally implicated in neuron and tissue injury after stroke, due to the function of supplying adenosine triphosphate (ATP) to the tissue, regulating oxidative metabolism during the pathologic process, and contribution to apoptotic cell death after stroke. As a catabolic mechanism, mitophagy links numbers of a complex network of mitochondria, and affects mitochondrial dynamic process, fusion and fission, reducing mitochondrial production of ROS, mediated by the mitochondrial permeability transition pore (MPTP). The precise nature of mitophagy’s involvement in stroke, and its underlying molecular mechanisms, have yet to be fully clarified. This review aims to provide a comprehensive overview of the integration of mitochondria with mitophagy, also to introduce and discuss recent advances in the understanding of the potential role, and possible signaling pathway, of mitophagy in the pathological processes of both hemorrhagic and ischemic stroke. The author also provides evidence to explain the dual role of mitophagy in stroke. - 中文關鍵字:
- 英文關鍵字: Mitochondria autophagy, Mitochondria, Stroke