Heart failure is a widespread chronic condition that directly impacts nearly six million Americans, contributes to almost one in ten deaths in the United States, and drains an estimated $30 billion annually from our national economy. Current treatments can slow progression of heart failure, but do not address the underlying issues, including the problem that causes systolic heart failure, the inability of the heart to pump blood throughout the body at normal levels.
Cardiac muscle contraction – the force that enables the heart to pump blood – is generated by interactions between actin and myosin, proteins that power movement at the molecular level by converting the molecule ATP into energy. Previous research from Dr. Mike Regnier’s lab has shown that dATP (a natural variant of ATP) can be used to promote stronger heart function, but there is a pressing need for data to explain why dATP helps to increase contractile force in heart disease.
Now, a recently-published study led by Dr. Regnier, Professor of Bioengineering, faculty member at the Institute for Stem Cell and Regenerative Medicine (ISCRM), and Director of the UW Center for Translational Muscle Research, offers new insights about the nature of dATP with unprecedented precision. The results are detailed in an article, authored by graduate student Joe Powers, appearing in the latest issue of the journal PNAS.
