Nicotinamide adenine dinucleotide phosphate oxidase activation and neuronal death after ischemic stroke
Jiamei Shen
Radhika Rastogi
Xiaokun Geng
Yuchuan Ding
摘要：Nicotinamide adenine dinucleotide phosphate oxidase (NOX) is a multisubunit enzyme complex that utilizes nicotinamide adenine dinucleotide phosphate to produce superoxide anions and other reactive oxygen species. Under normal circumstances, reactive oxygen species mediate a number of important cellular functions, including the facilitation of adaptive immunity. In pathogenic circumstances, however, excess reactive oxygen species generated by NOX promotes apoptotic cell death. In ischemic stroke, in particular, it has been shown that both NOX activation and derangements in glucose metabolism result in increased apoptosis. Moreover, recent studies have established that glucose, as a NOX substrate, plays a vital role in the pathogenesis of reperfusion injury. Thus, NOX inhibition has the potential to mitigate the deleterious impact of hyperglycemia on stroke. In this paper, we provide an overview of this research, coupled with a discussion of its implications for the development of NOX inhibition as a strategy for the treatment of ischemic stroke. Both inhibition using apocynin, as well as the prospect of developing more specific inhibitors based on what is now understood of the biology of NOX assembly and activation, will be highlighted in the course of our discussion.
机标关键词：
资助基金：This work was partially supported by Merit Review Award (I01RX-001964-01)as well as the National Natural Science Foundation of China(81501141)Beijing New Star of Science and Technology Program of China(xx2016061)Beijing Tongzhou District Financial Fund, and Scientifc Research Common Program of Beijing Municipal Commission of Education, China (KM201610025028)
论文发表日期：2019-01-01
在线出版日期：2025-08-15（本平台首次上网日期，不代表文献的发表时间）
页数：6( 948-953 )
英文信息