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J Clin Invest. 2012 Jan;122(1):30-2. doi: 10.1172/JCI61467. Epub 2011 Dec 27.

Redox redux: protecting the ischemic myocardium.

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Department of Medicine and Department of Pharmacology and Physiology, University of Rochester School of Medicine and Dentistry, Aab Cardiovascular Research Institute, Rochester, New York 14642, USA.


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.

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