Current treatments can slow progression of heart failure, but do not address the underlying issues, including specific problems that cause systolic heart failure. In this condition, the heart doesn’t contract vigorously enough in pushing blood into the body’s circulation.
The heart muscle contractions that pump blood are generated by interactions between actin and myosin. These motor proteins power movement at the molecular level by converting the molecule ATP into energy
Earlier research in the lab of Michael Regnier, UW professor of bioengineering, had shown that dATP, a natural variant of ATP, can be used to promote stronger heart function. However, there remains a pressing need for data to explain why dATP helps to increase contractile force in heart disease.
Now, a recently published study headed by Regnier, who is a researcher at the UW Medicine Institute for Stem Cell and Regenerative Medicine and director of the Center for Translational Muscle Research, offers new insights, with unprecedented precision, about the nature of dATP. The results are detailed in a report in the May 20 online edition of the journal PNAS. The first author of the paper is bioengineering graduate student Joseph D. Powers.
