Autonomous CaMKII Activity as a Drug Target for Histological and Functional Neuroprotection after Resuscitation from Cardiac Arrest

详细信息    查看全文

• 作者：Guiying Deng¹ ; ² ; James E. Orfila¹ ; ² ; Robert M. Dietz² ; ³ ; Myriam Moreno-Garcia¹ ; ² ; Krista M. Rodgers³ ; ⁴ ; Steve J. Coultrap⁴ ; Nidia Quillinan¹ ; ² ; Richard J. Traystman¹ ; ² ; ⁴ ; K. Ulrich Bayer⁴ ; ^{ulli.bayer@ucdenver.edu} ; Paco S. Herson¹ ; ² ; ⁴ ; ⁵ ; ^{paco.herson@ucdenver.edu}
• 关键词：CaMKII ; ischemia ; cardiac arrest ; tatCN19o ; neuroprotection ; LTP
• 刊名：Cell Reports
• 出版年：2017
• 出版时间：31 January 2017
• 年：2017
• 卷：18
• 期：5
• 页码：1109-1117
• 全文大小：2425 K
• 卷排序：18

文摘

CaMKII T286A mutation dramatically reduces neuronal injury after cardiac arrest CaMKII inhibition is neuroprotective when administered after cardiac arrest CaMKII inhibition protects in combination with therapeutic hypothermia Very low tatCN19o doses lead to anatomical and functional neuroprotection