Redox redux: protecting the ischemic myocardium.
Redox redux: protecting the ischemic myocardium.
复制标题
DOI：
10.1172/jci61467
复制
发表时间：
2012-01
期刊：
影响因子：
--
通讯作者：
Oded N. Spindel;B. Berk
中科院分区：
文献类型：
--
作者：
Oded N. Spindel;B. Berk
急性心肌梗死后，缺血心肌的血流迅速恢复时，会发生心脏缺血-再灌注（I-R）损伤。有趣的是，I-R损伤的许多特征与线粒体信号传导受损和线粒体功能障碍有关。因此，恢复心脏能量生物利用度和还原-氧化（氧化还原）信号传导在I-R损伤后的恢复中是重要的。在本期JCI中，Yoshioka及其同事描述了硫氧还蛋白相互作用蛋白（TXNIP）在控制线粒体呼吸和细胞能量代谢中的重要和意想不到的作用。他们的发现可能为开发TXNIP靶向治疗方法治疗心脏I-R损伤打开大门。
Cardiac ischemia-reperfusion (I-R) injury occurs upon prompt restoration of blood flow to the ischemic myocardium after an acute myocardial infarction. Interestingly, many of the features of I-R injury are related to impaired mitochondrial signaling and mitochondrial dysfunction. Restoring cardiac energy bioavailability and reduction-oxidation (redox) signaling are therefore important in recovery after I-R injury. In this issue of the JCI, Yoshioka and colleagues describe an important and unexpected role for thioredoxin-interacting protein (TXNIP) in the control of mitochondrial respiration and cell energy metabolism. Their findings could open the door for development of TXNIP-targeted therapeutic approaches for the treatment of cardiac I-R injury.