About 6.2 million Americans suffer from heart failure, an incurable disease with a staggering mortality rate – some 40 percent of patients die within five years of diagnosis. Heart failure is one form of heart disease, for which new therapies are desperately needed.
Now, in new work, scientists at the Lewis Katz School of Medicine (LKSOM) at Temple University identify a path to a promising novel therapeutic strategy, taking aim at a molecule in the heart known as G protein-coupled receptor kinase 5 (GRK5). In a study published online in the journal Cardiovascular Research, the scientists show in mice that reducing GRK5 levels can significantly improve survival following heart attack.
“Previous studies had found that GRK5 is elevated in patients with heart failure,” explained Claudio de Lucia, MD, PhD, an associate scientist in the Center for Translational Medicine at LKSOM and lead author on the new study. “Our new research, in mice that experienced myocardial infarction (heart attack), shows that GRK5 overexpression is associated with physiological changes in the heart that decrease cardiac function.”
Too much GRK5 in the heart was further linked to increased recruitment of immune cells into damaged heart tissue and harmful inflammation. The combination of these factors – reduced heart function and an influx of immune cells and inflammation – ultimately contributed to increased mortality in mice after heart attack.