期刊
CURRENT NEUROPHARMACOLOGY
卷 20, 期 7, 页码 1278-1296出版社
BENTHAM SCIENCE PUBL LTD
DOI: 10.2174/1570159X19666211101103646
关键词
Subarachnoid hemorrhage; mitochondria; early brain injury; delayed cerebral ischemia; oxidative stress; apoptosis; mitophagy
资金
- National Natural Science Foundation of China [81971107]
- Basic Public Welfare Research Project of Zhejiang Province [LGF19H090014]
Spontaneous subarachnoid hemorrhage (SAH) is a subtype of hemorrhagic stroke that places a heavy burden on health care. Early brain injury (EBI) may lay the foundation for further delayed cerebral ischemia (DCI) development and poor outcomes. Mitochondrial dysfunction is considered a novel mechanism related to DCI and post-SAH outcomes.
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 (Delta psi m) 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.
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