Richard Austin, PhD, and a team of researchers are studying the cellular and molecular mechanisms that accelerate the development and progression of atherosclerosis, the underlying cause of cardiovascular disease and stroke. These studies have provided important clues as to how changes in cell function contribute to this progressive and life threatening disease.
Dr. Austin, a professor in the department of Pathology and Molecular Medicine and a Career Investigator of the Heart and Stroke Foundation of Ontario, said the study found that nitric oxide, normally considered a "good player" in protection against atherosclerosis, could sometimes be converted into a toxic byproduct with a detrimental impact on cell viability and function.
"The results from our study show that under the right cellular conditions, such as the increased production of cellular oxidants, nitric oxide can be converted into a very "bad player", namely peroxynitrite," said Dr. Austin, a Staff Scientist who works at the Henderson Research Centre.
"Although previous reports have demonstrated that the generation of peroxynitrite in the vessel wall accelerates atherosclerosis, the cellular mechanism responsible for this effect was relatively unknown. Our study shows that the production of peroxynitrite causes cell dysfunction and death by activating or 'turning on' a cellular stress pathway, termed the ER stress response pathway.