Mechanisms and potential therapeutic targets for spontaneous intracerebral hemorrhage

被引:18
作者
Hua, Wei [1 ]
Chen, Xuemei [2 ]
Wang, Junmin [2 ]
Zang, Weidong [2 ]
Jiang, Chao [3 ]
Ren, Honglei [4 ]
Hong, Michael [5 ]
Wang, Jiarui [6 ]
Wu, He [1 ]
Wang, Jian [2 ]
机构
[1] Harbin Med Univ, Clin Hosp 1, Dept Pathol, Harbin 150001, Heilongjiang, Peoples R China
[2] Zhengzhou Univ, Dept Human Anat, Basic Med Coll, Zhengzhou 450001, Henan, Peoples R China
[3] Zhengzhou Univ, Dept Neurol, Affiliated Hosp 5, Zhengzhou 450052, Henan, Peoples R China
[4] Tianjin Med Univ, Gen Hosp, Dept Neurol, Tianjin 300053, Peoples R China
[5] Univ Maryland, Sch Med, Baltimore, MD 21201 USA
[6] Johns Hopkins Univ, Baltimore, MD 21218 USA
基金
中国国家自然科学基金;
关键词
Ferroptosis; Heme oxygenase; Intracerebral hemorrhage; Iron toxicity; Prostaglandin E2; INHIBITS HMGB1 PHOSPHORYLATION; BRAIN-INJURY; INFLAMMATORY MEDIATORS; NEURONAL DEATH; EP2; RECEPTOR; MOUSE MODEL; TIME-COURSE; CELL-DEATH; IRON; FERROPTOSIS;
D O I
10.1016/j.hest.2020.02.002
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
In this review paper, the most recent research on intracerebral hemorrhage (ICH) is summarized and novel perspectives are offered on the pathomechanisms of ICH. These underlying pathomechanisms of ICH provide clues for development of novel drugs or drug target screening. Specifically, recent research has provided evidence that iron chelators, lipid peroxidation/ferroptosis inhibitors, agonists or antagonists of prostaglandin E2 receptors (EP1/3 or EP2), and nonsteroidal anti-inflammatory drugs protect against ICH-induced brain edema, secondary brain tissue damage as well as inhibition of the toxicity in related tissue damage products. This review will provide a theoretical basis for testing new compounds that may have potential for future clinical trials.(c) 2020 Production and hosting by Elsevier B.V. on behalf of KeAi Communications Co., Ltd. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).
引用
收藏
页码:99 / 104
页数:6
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