Alterations in Copper Homeostasis in Ischemic Heart Disease
Alterations in Copper Homeostasis in Ischemic Heart Disease
WASHINGTON, May 30, 2018 /PRNewswire/ -- An article published in Experimental Biology and Medicine (Volume 243, Issue 9, May 2018) answers a long-standing clinical question regarding elevated blood copper levels in patients with myocardial ischemia (http://journals.sagepub.com/doi/full/10.1177/1535370218773055). The study, led by Dr. Y. James Kang in the Regenerative Medicine Research Center at Sichuan University West China Hospital in Chengdu, China, reports that copper is released from the heart into the blood in a mouse model of myocardial ischemia.
Myocardial ischemia is very common, with over three million cases each year in the U.S. alone. Myocardial ischemia occurs when blood flow to the heart is reduced and the heart muscle (myocardium) does not receive enough oxygen to function normally. It has been known for many years that patients with myocardial ischemia have elevated levels of copper in the blood. However, the mechanism by which this occurs is not known. Reduced copper levels in the ischemic heart suggest that ischemic injury may cause the heart to release copper into the blood. But there is no direct evidence that the heart releases copper and if so, whether the amount released is sufficient to sustain the elevated blood copper levels in patients. Answering this long-standing clinical question regarding copper homeostasis would aid the diagnosis and treatment of myocardial ischemia.
The study by Dr. Kang and colleagues examines copper homeostasis in a mouse model of myocardial ischemia. After injury, myocardial copper concentrations continuously decreased while copper concentrations in the blood continually increased. These changes were accompanied by increased levels of myocardial COMMD1, a copper chaperone responsible for transferring copper from inside of the cell to an outside environment. Dr. Kang said that "We are excited to have worked out the cause-and-effect relationship between myocardial copper efflux and the elevation of serum copper concentrations, addressing a long-term clinical question. As important, we found that a copper chaperone is involved in the release of myocardial copper. This will help us further define the mechanism of myocardial copper efflux, a long-term puzzle."
Dr. Steven R. Goodman, editor-in-chief of Experimental Biology & Medicine, said "Kang and colleagues have made a major contribution to our understanding of copper efflux from the ischemic heart with concurrent elevation in the blood. This important study indicates that upregulation of copper metabolism MURR domain 1 (COMMD1) plays a critical role in this process."
Experimental Biology and Medicine is a journal dedicated to the publication of multidisciplinary and interdisciplinary research in the biomedical sciences. The journal was first established in 1903. Experimental Biology and Medicine is the journal of the Society of Experimental Biology and Medicine. To learn about the benefits of society membership, visit www.sebm.org. For anyone interested in publishing in the journal, please visit http://ebm.sagepub.com/.
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SOURCE Experimental Biology and Medicine
