Search:


Hesperadin Is a Novel CaMKII-δ Inhibitor Hesperadin Exerts Dual Functions to Ameliorate Cardiac Ischemia/Reperfusion Injury and Inhibit Tumor Growth


Junxia Zhang; Ruqi Liang; Kai Wang; Wenjia Zhang; Mao Zhang; Li Jin; Peng Xie; Wen Zheng; Haibao Shang; Qingmei Hu; Jiayi Li; Gengjia Chen; Fujian Wu; Feng Lan; Lipeng Wang; Shi-Qiang Wang; Yongfeng Li; Yong Zhang; Jinghao Liu; Fengxiang Lv; Xinli Hu; Rui-Ping Xiao; Xiaoguang Lei; Yan Zhang.

Circulation 2022, 145, 1154-1168

Cardiac ischemia/reperfusion (I/R) injury has emerged as an important therapeutic target for ischemic heart disease, the leading cause of morbidity and mortality worldwide. At present, there is no effective therapy for reducing cardiac I/R injury. CaMKII (Ca2+/calmodulin-dependent kinase II) plays a pivotal role in the pathogenesis of severe heart conditions, including I/R injury. Pharmacological inhibition of CaMKII is an important strategy in the protection against myocardial damage and cardiac diseases. To date, there is no drug targeting CaMKII for the clinical therapy of heart disease. Furthermore, at present, there is no selective inhibitor of CaMKII-δ, the major CaMKII isoform in the heart.

Junxia Zhang; Ruqi Liang; Kai Wang; Wenjia Zhang; Mao Zhang; Li Jin; Peng Xie; Wen Zheng; Haibao Shang; Qingmei Hu; Jiayi Li; Gengjia Chen; Fujian Wu; Feng Lan; Lipeng Wang; Shi-Qiang Wang; Yongfeng Li; Yong Zhang; Jinghao Liu; Fengxiang Lv; Xinli Hu; Rui-Ping Xiao; Xiaoguang Lei; Yan Zhang.

Circulation 2022, 145, 1154-1168

Cardiac ischemia/reperfusion (I/R) injury has emerged as an important therapeutic target for ischemic heart disease, the leading cause of morbidity and mortality worldwide. At present, there is no effective therapy for reducing cardiac I/R injury. CaMKII (Ca2+/calmodulin-dependent kinase II) plays a pivotal role in the pathogenesis of severe heart conditions, including I/R injury. Pharmacological inhibition of CaMKII is an important strategy in the protection against myocardial damage and cardiac diseases. To date, there is no drug targeting CaMKII for the clinical therapy of heart disease. Furthermore, at present, there is no selective inhibitor of CaMKII-δ, the major CaMKII isoform in the heart.