News Release

Georgia State researcher gets $2.4 million federal grant to study diabetic vascular diseases

Grant and Award Announcement

Georgia State University

Ming-Hui Zou, Georgia State University

image: This is Dr. Ming-Hui Zou, director of the Center for Molecular and Translational Medicine at Georgia State University. view more 

Credit: Georgia State University

ATLANTA--Dr. Ming-Hui Zou, director of the Center for Molecular and Translational Medicine at Georgia State University, has received a four-year, $2.4 million federal grant to study cardiovascular complications in diabetes.

The grant from the National Heart, Lung and Blood Institute of the National Institutes of Health allows Zou to continue his research, which has been funded since 2004.

The study will investigate how high glucose promotes dysfunction of mitochondria, the cell structures that produce the energy cells need to survive. It will also explore how mitochondrial fission, or division into two or more independent structures, results in atherosclerosis, the buildup of fats, cholesterol and other substances in and on the artery walls, and dysfunction of endothelial cells, which line the interior surface of blood vessels and lymphatic vessels.

Studies show that mitochondria play a causative role in diabetic endothelial dysfunction, though it's unclear how the mitochondria become dysfunctional.

"There's a single layer of cells in the vasculature, which is called endothelial cells. These cells are very important," Zou said. "They separate the circulating blood and the organs, so they protect the organs from damage. It's like a barrier to prevent the blood going into the tissue. We study how this type of cells would become dysfunctional or damaged.

"We are also looking at how the defense of this cell type could prevent the damage caused by diabetes or hyperglycemia, high blood sugar concentration. We found the cells have a mechanism called autophagy, or self-eating, in which they digest themselves under stress conditions. It's like an internal self-defense mechanism. We're studying how this mechanism becomes dysfunctional and how we can enhance this part of the function to protect these cells and result in increased resistance to disease conditions."

An abstract of the grant, 2R01HL079584-16, is available at the NIH's Project RePORTER website.

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