{"title":"线粒体电压依赖性阴离子通道、Bcl-2家族蛋白和c-Jun n端激酶在缺血性卒中相关细胞凋亡中的作用","authors":"Rajeev Gupta , Subhendu Ghosh","doi":"10.1016/j.biopen.2017.02.002","DOIUrl":null,"url":null,"abstract":"<div><p>There is a constant need for better stroke treatments. Neurons at the periphery of an ischemic stroke affected brain tissue remains metabolically active for several hours or days after stroke onset. They later undergo mitochondrion-mediated apoptosis. It has been found that inhibiting apoptosis in the peripheral ischemic neurons could be very effective in the prevention of stroke progression. During stroke associated apoptosis, cytosolic c-Jun N-terminal Kinases (JNKs) and Bcl-2 family proteins translocate towards mitochondria and promote cytochrome <em>c</em> release by interacting with the outer mitochondrion membrane associated proteins. This review provides an overview of the plausible interactions of the outer mitochondrial membrane Voltage Dependent Anion Channel, Bcl-2 family proteins and JNKs in cytochrome <em>c</em> release in the peripheral ischemic stroke associated apoptotic neurons. The review ends with a note on designing new anti-stroke treatments.</p></div>","PeriodicalId":92004,"journal":{"name":"Biochimie open","volume":null,"pages":null},"PeriodicalIF":0.0000,"publicationDate":"2017-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.biopen.2017.02.002","citationCount":"28","resultStr":"{\"title\":\"Putative roles of mitochondrial Voltage-Dependent Anion Channel, Bcl-2 family proteins and c-Jun N-terminal Kinases in ischemic stroke associated apoptosis\",\"authors\":\"Rajeev Gupta , Subhendu Ghosh\",\"doi\":\"10.1016/j.biopen.2017.02.002\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<div><p>There is a constant need for better stroke treatments. Neurons at the periphery of an ischemic stroke affected brain tissue remains metabolically active for several hours or days after stroke onset. They later undergo mitochondrion-mediated apoptosis. It has been found that inhibiting apoptosis in the peripheral ischemic neurons could be very effective in the prevention of stroke progression. During stroke associated apoptosis, cytosolic c-Jun N-terminal Kinases (JNKs) and Bcl-2 family proteins translocate towards mitochondria and promote cytochrome <em>c</em> release by interacting with the outer mitochondrion membrane associated proteins. This review provides an overview of the plausible interactions of the outer mitochondrial membrane Voltage Dependent Anion Channel, Bcl-2 family proteins and JNKs in cytochrome <em>c</em> release in the peripheral ischemic stroke associated apoptotic neurons. The review ends with a note on designing new anti-stroke treatments.</p></div>\",\"PeriodicalId\":92004,\"journal\":{\"name\":\"Biochimie open\",\"volume\":null,\"pages\":null},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2017-06-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://sci-hub-pdf.com/10.1016/j.biopen.2017.02.002\",\"citationCount\":\"28\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Biochimie open\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://www.sciencedirect.com/science/article/pii/S2214008517300032\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Biochimie open","FirstCategoryId":"1085","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S2214008517300032","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 28
摘要
人们一直需要更好的中风治疗方法。缺血性中风影响的脑组织周围的神经元在中风发作后数小时或数天内仍保持代谢活跃。它们随后经历线粒体介导的细胞凋亡。研究发现,抑制外周缺血神经元的细胞凋亡可以非常有效地预防脑卒中的进展。在卒中相关凋亡过程中,胞质c- jun n -末端激酶(JNKs)和Bcl-2家族蛋白向线粒体转运,并通过与线粒体外膜相关蛋白相互作用促进细胞色素c的释放。本文综述了线粒体外膜电压依赖性阴离子通道、Bcl-2家族蛋白和JNKs在外周缺血性卒中相关凋亡神经元细胞色素c释放中的可能相互作用。回顾以设计新的抗中风治疗方法的注释结束。
Putative roles of mitochondrial Voltage-Dependent Anion Channel, Bcl-2 family proteins and c-Jun N-terminal Kinases in ischemic stroke associated apoptosis
There is a constant need for better stroke treatments. Neurons at the periphery of an ischemic stroke affected brain tissue remains metabolically active for several hours or days after stroke onset. They later undergo mitochondrion-mediated apoptosis. It has been found that inhibiting apoptosis in the peripheral ischemic neurons could be very effective in the prevention of stroke progression. During stroke associated apoptosis, cytosolic c-Jun N-terminal Kinases (JNKs) and Bcl-2 family proteins translocate towards mitochondria and promote cytochrome c release by interacting with the outer mitochondrion membrane associated proteins. This review provides an overview of the plausible interactions of the outer mitochondrial membrane Voltage Dependent Anion Channel, Bcl-2 family proteins and JNKs in cytochrome c release in the peripheral ischemic stroke associated apoptotic neurons. The review ends with a note on designing new anti-stroke treatments.