Mitochondria: Novel Mechanisms and Therapeutic Targets for Secondary Brain Injury After Intracerebral Hemorrhage.
Mitochondria: Novel Mechanisms and Therapeutic Targets for Secondary Brain Injury After Intracerebral Hemorrhage.
复制标题
线粒体：脑出血后继发性脑损伤的新机制和治疗靶点。
DOI：
10.3389/fnagi.2020.615451
复制
发表时间：
2020
影响因子：
4.8
通讯作者：
Chen Y
中科院分区：
文献类型：
--
作者：
Chen W;Guo C;Feng H;Chen Y
脑出血（ICH）是一种破坏性形式的中风，往往导致死亡或残疾。然而，幸存者通常会出现神经损伤和精神障碍的后遗症，影响他们的日常功能和工作能力。近期的MISTIE III和斯蒂奇II试验证实早期手术清除血肿并不能改善脑出血存活者的预后，因此寻找脑出血后继发性脑损伤（SBI）的干预靶点至关重要。氧化应激、神经炎症和自噬等可能引起的线粒体功能障碍被认为是脑出血的一种新的病理机制。此外，线粒体在出血性卒中后促进神经元存活和改善神经功能方面发挥重要作用。本文综述了脑出血中线粒体参与细胞死亡、活性氧产生、炎症激活、血脑屏障破坏和脑水肿的机制。我们强调线粒体保护作为脑卒中后SBI潜在治疗靶点的潜力，并为临床策略提供有价值的见解。
Intracerebral hemorrhage (ICH) is a destructive form of stroke that often results in death or disability. However, the survivors usually experience sequelae of neurological impairments and psychiatric disorders, which affect their daily functionality and working capacity. The recent MISTIE III and STICH II trials have confirmed that early surgical clearance of hematomas does not improve the prognosis of survivors of ICH, so it is vital to find the intervention target of secondary brain injury (SBI) after ICH. Mitochondrial dysfunction, which may be induced by oxidative stress, neuroinflammation, and autophagy, among others, is considered to be a novel pathological mechanism of ICH. Moreover, mitochondria play an important role in promoting neuronal survival and improving neurological function after a hemorrhagic stroke. This review summarizes the mitochondrial mechanism involved in cell death, reactive oxygen species (ROS) production, inflammatory activation, blood–brain barrier (BBB) disruption, and brain edema underlying ICH. We emphasize the potential of mitochondrial protection as a potential therapeutic target for SBI after stroke and provide valuable insight into clinical strategies.
登录
查看更多内容
影响因子：
82.9
作者：
Cloonan SM;Glass K;Laucho-Contreras ME;Bhashyam AR;Cervo M;Pabón MA;Konrad C;Polverino F;Siempos II;Perez E;Mizumura K;Ghosh MC;Parameswaran H;Williams NC;Rooney KT;Chen ZH;Goldklang MP;Yuan GC;Moore SC;Demeo DL;Rouault TA;D'Armiento JM;Schon EA;Manfredi G;Quackenbush J;Mahmood A;Silverman EK;Owen CA;Choi AM
通讯作者：
Choi AM
影响因子：
8.3
作者：
Chou SH;Lan J;Esposito E;Ning M;Balaj L;Ji X;Lo EH;Hayakawa K
通讯作者：
Hayakawa K
HEERPUD1表达增加参与脑出血后神经元凋亡
影响因子：
3.8
作者：
Ding, Wensen;Chen, Rongrong;Shen, Lihua
通讯作者：
Shen, Lihua
影响因子：
21.3
作者：
Eisner V;Picard M;Hajnóczky G
通讯作者：
Hajnóczky G
影响因子：
4.2
作者：
Chinopoulos, Christos
通讯作者：
Chinopoulos, Christos