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Researchers at Emory University School of Medicine have identified hepcidin, a hormone that regulates iron levels in the body, as a potential target for treating atherosclerosis.
Suppressing hepcidin is a way to reduce the iron levels inside the white blood cells found in arterial plaques. Reducing iron levels pushes those cells to clean up harmful cholesterol in a process called “reverse cholesterol transport,” interfering with atherosclerosis, researchers have found.
The data was presented Wednesday, Nov. 16 by Aloke Finn, MD, assistant professor of medicine (cardiology) and colleague Omar Saeed at the American Heart Association Scientific Sessions meeting in Orlando. Charles Hong, MD, PhD, from Vanderbilt University and collaborators from CVPath Institute contributed to the research.
Update: The results were published online in the American Heart Association journal ATVB (Arteriosclerosis, Thrombosis and Vascular Biology) on Nov. 17.
When mice modeling atherosclerosis are given a compound that reduces hepcidin levels, they have smaller atherosclerotic plaques and less fat in their plaques, as well as reduced foam cell formation. Foam cells are macrophages (white blood cells) that accumulate cholesterol and are signs of atherosclerosis.
The compound LDN 193189 reduces hepcidin levels by blocking its production. LDN 193189 is also being investigated as a treatment for inflammatory bowel disease and for anemia related to critical illness.
In the ATVB paper, the authors caution that therapies that reduce hepcidin need to be evaluated for whether they result in hemochromatosis (iron overload): "Although multiple mechanisms exist within humans to counteract iron-related toxicity..., it remains possible that such toxicity could be a limitation to the actual clinical adoption of such a strategy."
At the meeting, Finn also presented research on how hemoglobin, the iron-containing protein that allows red blood cells to carry oxygen, affects macrophages. He and his colleagues used isolated human cells and a rabbit model of atherosclerosis to show that macrophages respond to hemoglobin by increasing production of proteins that transport cholesterol and pump iron out.
In the context of atherosclerosis, iron is toxic because it amplifies the action of reactive oxygen species, leading to more inflammation and more foam cells. Previous research has shown that hemorrhage within atherosclerotic plaques, leading to the release of hemoglobin from red blood cells, is linked to enlargement of the plaque’s necrotic core a sign of “vulnerable plaque.”
“We were led to the hepcidin research by our work on macrophages,” Finn says. “We discovered a different type of macrophages that detoxify iron. They take it up and spit it out again with ferroportin, an iron transport protein.”
“Hemorrhage is bad, but as bad at it is, these macrophages seem to protect against the toxic effects of iron. Giving macrophages hemoglobin encourages them to behave in this detox mode,” he says.
This study was supported by the Carlyle Fraser Heart Center, CVPath Inc., and the National Institutes of Health. It is possible that Finn and Emory could benefit financially from this technology’s future commercialization.
The Robert W. Woodruff Health Sciences Center of Emory University is an academic health science and service center focused on missions of teaching, research, health care and public service.