Related Experiment Video
Updated: May 26, 2026

Improved Rodent Model of Myocardial Ischemia and Reperfusion Injury
Published on: March 7, 2022
Redox redux: protecting the ischemic myocardium
Oded N Spindel1, Bradford C Berk
1Department 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.
Abstract:
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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