Maintaining Heart Function After a Heart Attack

An article published in Experimental Biology and Medicine (Volume 246, Issue 5, March, 2021) ( reports a new therapeutic option for preventing long-term damage to the heart after a heart attack. The study, led by Dr. Y. James Kang, in the Regenerative Medicine Research Center at Sichuan University in Chengdu (China) and the Memphis Institute of Regenerative Medicine at the University of Tennessee Health Science Center in Memphis, TN (USA), reports that inhibition of the copper chaperone COMMD1 blocks myocardial injury and maintains heart function in a mouse model of myocardial ischemia.
Heart attack not only causes instant chest pain and discomfort but also leads to a long-term ischemic injury to the heart that can result in a heart failure. In the process of myocardial ischemic infarction, an essential trace element copper is pushed out from the heart. Previous studies have demonstrated that repletion of copper to the copper-deficient ischemic heart can repair the damaged heart and facilitate recovery of heart function. Therefore, it is possible that preventing copper efflux from the heart after ischemic injury would block long-term damage to the heart. Before this treatment option can be evaluated, the following questions must be answered: how is copper exported from the heart, and how can copper efflux from the ischemic heart be prevented?
In this study, Kang and colleagues examined the role of the intracellular copper chaperone COMMD1 in a mouse model of myocardial ischemia. Genetic deletion of the COMMD1 gene in the heart blocked copper loss from the heart after ischemic insult. Importantly, prevention of copper loss from the heart remarkably suppressed heart tissue death and preserved heart function. Dr. Kang said “We are excited to answer a long-lasting question related to copper loss from the heart under ischemic conditions, an observation that was made more than two decades ago. With the solving of this puzzle, we are moving forward towards an alternative approach to the treatment of patients with ischemic heart disease.”
Dr. Steven R. Goodman, Editor-in-Chief of Experimental Biology & Medicine, said, “Dr. Kang and colleagues have provided elegant studies demonstrating that cardiomyocyte-specific conditional deletion of the copper chaperone protein COMMD1 significantly prevents copper loss in the ischemic myocardium, leading to preservation of myocardial contractile function. This offers the possibility that modulation of COMMD1 may provide a new therapeutic target for the treatment of myocardial ischemic injury.”
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Source: Experimental Biology and Medicine