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Scientists Elucidate Molecular Pathway Driving Maladaptive Processes in Heart Failure

Poor survival after heart attack linked to excess levels of signaling protein in heart

 E-Mail (Philadelphia, PA) - 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.

Temple researchers identify cardiac protein that causes different types of heart failure

 E-Mail (Philadelphia, PA) - Like a failing fuel pump that causes a loss of engine power in a car, a diseased heart can take a serious toll on the body s performance. For some patients, tasks like walking up a flight of stairs or walking across a room eventually turn into exhausting endeavors. This is because, over time, regardless of the underlying cause, heart damage typically progresses, owing to a constant barrage of oxidative stress and toxic lipids that alter heart cell energetics and, ultimately, the ability of the heart to function normally. Oxidative stress occurs when harmful oxygen-containing molecules outnumber helpful antioxidants, leading to damaging reactions with proteins, DNA, and other cell components. Now, in two new studies, researchers at the Lewis Katz School of Medicine at Temple University (LKSOM) show that in the heart, one molecule in particular, Kruppel-like factor (KLF)-5, single-handedly fuels both the generation of oxidizing molecules and the accumul

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