Aging is the single greatest risk factor for most chronic diseases, including heart disease. As we age, the risk of heart disease and heart failure rises, driven by factors such as stiff or blocked blood vessels, inflammation, faulty heart valves, irregular heart rhythms, changes in cellular composition, and the heart’s reduced ability to beat rapidly during physical activity or stress. A key hallmark of aging and one component of heart disfunction is mitochondrial damage. Mitochondria, commonly known as our cells’ “power plants,” also play a key role in the way our cells adapt to stress. As we age, our heart mitochondria perform less effectively, leading to changes in the heart’s structure and function. However, the link between these changes in the mitochondria and increased risk for heart disease remains unknown. As a result, there is a lack of proven treatments that target mitochondria to support the aging heart.
Two UW professors are collaborating to study mitochondrial damage in the heart and treatment with the natural supplement urolithin A (UA). The primary investigators are Michael Regnier, professor of Bioengineering, a faculty member in the Institute for Stem Cell and Regenerative Medicine (ISCRM), and the director of the UW Center for Translational Muscle Research (CTMR); and David Marcinek, professor of Radiology and Laboratory Medicine and Pathology, adjunct professor of Bioengineering, co-director of the Nathan Schock Center of Excellence in Basic Biology of Aging at UW, and also a faculty member in ISCRM and CTMR. Regnier and Marcinek have a history of collaborating on projects that examine small molecules. This partnership will advance Regnier’s goal to increase aging muscle research both in the Regnier lab and the CTMR and Marcinek’s goal of connecting fundamental aging research with the outstanding disease focused research at the UW.
