粒体自噬
医学
神经炎症
兴奋毒性
蛛网膜下腔出血
氧化应激
线粒体
活性氧
神经科学
冲程(发动机)
血管痉挛
细胞生物学
生物信息学
细胞凋亡
炎症
麻醉
自噬
内科学
谷氨酸受体
生物
受体
生物化学
工程类
机械工程
作者
Zeyu Zhang,Anke Zhang,Yibo Liu,Xiaoming Hu,Yuanjian Fang,Xiaoyu Wang,Yue Luo,Cameron Lenahan,Sheng Chen
出处
期刊:Current Neuropharmacology
[Bentham Science]
日期:2022-07-01
卷期号:20 (7): 1278-1296
被引量:13
标识
DOI:10.2174/1570159x19666211101103646
摘要
Spontaneous subarachnoid hemorrhage (SAH) accounts for 5-10% of all strokes and is a subtype of hemorrhagic stroke that places a heavy burden on health care. Despite great progress in surgical clipping and endovascular treatment for ruptured aneurysms, cerebral vasospasm (CVS) and delayed cerebral ischemia (DCI) threaten the long-term outcomes of patients with SAH. Moreover, there are limited drugs available to reduce the risk of DCI and adverse outcomes in SAH patients. New insight suggests that early brain injury (EBI), which occurs within 72 h after the onset of SAH, may lay the foundation for further DCI development and poor outcomes. The mechanisms of EBI mainly include excitotoxicity, oxidative stress, neuroinflammation, blood-brain barrier (BBB) destruction, and cellular death. Mitochondria are a double-membrane organelle, and they play an important role in energy production, cell growth, differentiation, apoptosis, and survival. Mitochondrial dysfunction, which can lead to mitochondrial membrane potential (Δψm) collapse, overproduction of reactive oxygen species (ROS), release of apoptogenic proteins, disorders of mitochondrial dynamics, and activation of mitochondria-related inflammation, is considered a novel mechanism of EBI related to DCI as well as post-SAH outcomes. In addition, mitophagy is activated after SAH. In this review, we discuss the latest perspectives on the role of mitochondria in EBI and DCI after SAH. We emphasize the potential of mitochondria as therapeutic targets and summarize the promising therapeutic strategies targeting mitochondria for SAH.
科研通智能强力驱动
Strongly Powered by AbleSci AI