Metabolic molecule impedes wound healing, study finds
Zoltan Arany, M.D.
Poor wound healing can lead to amputations, or worse. New findings have helped unearth what happens to tiny blood vessels in the body to slow wound healing in diabetics.
Researchers at Beth Israel Deaconess Medical Center have discovered a molecule called PGC-1alpha — which has previously been shown to spur the growth of blood vessels in muscle — has the opposite effect in the endothelial cells of patients with diabetes. As a result, such residents face impaired blood vessel growth that can lead to dangerous vascular complications.
“Diabetes is the number one cause of amputations in the U.S.,” noted senior author Zoltan Arany, M.D., Ph.D., an investigator in BIDMC's CardioVascular Institute and Associate Professor of Medicine at Harvard Medical School. “While it's been believed that high levels of glucose were somehow to blame for the inability of chronic ulcers and infections to properly heal in these patients, it wasn't completely understood how this was happening.”
With this new research, Arany says, it is apparent that high levels of blood glucose — the hallmark of diabetes — induce high levels of the PGC-1 alpha molecule in the endothelial cells lining the blood vessels. This, in turn, prevents endothelial cells from properly functioning, inhibiting blood vessel growth.
Full findings appear in the journal Cell Metabolism.