Redox redux: protecting the ischemic myocardium.
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.
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.
Oded N
ON
Spindel
Bradford C
BC
Berk
D000818:Animals; D002352:Carrier Proteins / Q000037:antagonists & inhibitors* / Q000235:genetics*; D005260:Female; D006801:Humans; D008297:Male; D008929:Mitochondria, Heart / Q000378:metabolism*; D015428:Myocardial Reperfusion Injury / Q000378:metabolism* / Q000517:prevention & control*; D013879:Thioredoxins / Q000037:antagonists & inhibitors* / Q000235:genetics*
D002352:Carrier Proteins; C445672:Txnip protein, mouse; D013879:Thioredoxins