Xiangyu Zhang1,2 · Yan Zhang1,2 · Qiuyang Su1,2 · Yang Liu1,2 · Zhe Li1,2 · V. Wee Yong3 · Mengzhou Xue1,21 Department of Cerebrovascular Diseases, The Second Afliated Hospital of Zhengzhou University, Zhengzhou 450000, China
2 Academy of Medical Science, Zhengzhou University, Zhengzhou 450000, China
3 Hotchkiss Brain Institute and Department of Clinical Neurosciences, University of Calgary, Calgary, AB T2N 1N4, Canada
Abstract
Injury to the brain after intracerebral hemorrhage (ICH) results from numerous complex cellular mechanisms. At present, effective therapy for ICH is limited and a better understanding of the mechanisms of brain injury is necessary to improve prognosis. There is increasing evidence that ion channel dysregulation occurs at multiple stages in primary and secondary brain injury following ICH. Ion channels such as TWIK-related K+ channel 1, sulfonylurea 1 transient receptor potential melastatin 4 and glutamate-gated channels affect ion homeostasis in ICH. They in turn participate in the formation of brain edema, disruption of the blood-brain barrier, and the generation of neurotoxicity. In this review, we summarize the interaction between ions and ion channels, the effects of ion channel dysregulation, and we discuss some therapeutics based on ion-channel modulation following ICH.
Keywords
Intracerebral hemorrhage; Ion dyshomeostasis; Sulfonylurea 1 transient receptor potential melastatin 4; TWIK-related K+ channel 1; N-methyl-Daspartate receptor; Transient receptor potential vanilloid 4
