Joon Young Park, assistant professor of kinesiology and director of Temple’s Cardiovascular Genomics Laboratory, has made a career of studying the human circulatory system. Now Park and his colleagues are investigating how certain proteins may mimic the effect of aerobic exercise, and thereby prevent cardiovascular disease.
“Mitochondria consume oxygen and generate energy,” said Park. Many diseases, Park continued, are correlated with mitochondria dysfunction, which can trigger or accelerate cell death processes. “When scientists like me analyze blood vessels with certain conditions like hypertension, diabetes, cardiovascular disease, or even coronary artery disease, we find that the mitochondria found in that diseased tissue is itself dysfunctional.”
“What if we could improve mitochondrial function? Could it be beneficial to the blood vessel, or perhaps reduce or prevent disease development?”
Park said that while it is well known that exercise benefits the vascular system, researchers don’t know specifically how that happens, which is why he has been studying the effect of exercise on the cellular level for the past six years. “When we exercise, we burn calories, which in turn increases blood flow into that area of the body. In a previous study we simulated these changes in blood flow to stimulate the vascular cells, and what we found was an increase in mitochondria content, integrity, and dynamic behavior.”
In the current project, Park and his team have received a $2.5 million from the National Heart Blood Lung Institute (NHBLI) to research the functional implications of this discovery, and in particular the role of a potentially important protein known as P53. “P53 protein already exists in the cell,” he said. “This protein is absorbed into the mitochondria of blood vessel cells when an individual exercises. In the new study, we’re collaborating with National Institute of Health investigators to study the role of P53 once it’s been absorbed.”
There are a few reasons for this line of inquiry, Park said. For example, simply knowing the molecular mechanism that underlies the benefits to the vascular system can motivate able-bodied patients to participate in regular exercise. “But more importantly, we are hoping to develop a drug which can benefit the vascular system, by mimicking the effects of exercise on the vascular mitochondria. This could help cure cardiovascular disease in the future, including among people incapable of physical exercise.”