Understanding How Oxidative Stress Impairs Endothelial Progenitor Cell Function May Lead to Antioxidant Therapy to Prevent Cardiovascular Disease
IU School of Medicine Nov 25, 2008
Researchers from the Herman B Wells Center for Pediatric Research at the Indiana University School of Medicine and Riley Hospital for Children report in the November 2008 issue of the journal Antioxidants & Redox Signaling that a review of the scientific literature reveals that how EPCs respond to oxidantive stress appears to be a critical determinant in maintaining a healthy cardiovascular system.
A comprehensive understanding of how oxidative stress, the biochemical modification of cells, impairs EPC function may lead to antioxidant therapy to prevent disease.
“The study of EPCs is exciting because as the work evolves it should enable us to develop clinical strategies to decrease the risk of heart attack or stroke by reversing oxidative stress at the cellular level,” said study author Laura Haneline, M.D., associate professor of pediatrics at the IU School of Medicine. “These strategies will need to be applied early in the disease when preventing oxidative damage is a possibility because once the damage has occurred it may not be reversible.”
High cholesterol causes increased oxidative stress, impairing the function of EPCs. In addition to being implicated in cardiovascular diseases, oxidative stress is also a factor in diabetes.
“Further studies of how oxidative stress impairs the function of EPCs are critical. Eventually you should be able to get a simple blood test measuring your EPCs to see if you are at risk for disease. With this knowledge, in the not too distant future, we should be able to apply antioxidant therapies to prevent that disease,” said Dr. Haneline.
In the meantime studies that examine the impact of oxidative stress on specific functions of the EPCs are needed to fully understand the progression of vascular disease.
A neonatologist at Riley Hospital, Dr. Haneline became interested in EPCs because it is in the fetal in utero environment that these cells are programmed. Co-authors of the study, which was funded by the National Institutes of Health, are Jamie Case, Ph.D. and David A. Ingram, M.D. of the IU School of Medicine and Riley Hospital.