Clinicians and scientists have long observed that cells in overstressed hearts have high levels of the simple sugar O-GlcNAc modifying thousands of proteins within cells.
In a new study from Johns Hopkins Medicine, researchers found evidence that these excess sugars could well be a cause, not merely a consequence or marker of heart failure.
They found that elevated levels of O-GlcNAc increased the risk of heart failure, but lowering levels of O-GlcNAc reduced the risk of death and got heart function to normal.
The findings could offer a potentially new therapy that prevents or stops heart failure.
According to the Centers for Disease Control and Prevention, an estimated 6.2 million Americans have heart failure, a progressive condition in which the heart struggles and ultimately fails to pump enough blood and oxygen to support the body’s organs.
Other conditions, including high blood pressure, diabetes and obesity contribute to the development of heart failure.
Previous research has shown that proteins in the cells of people with heart failure have more O-GlcNAc than usual.
In the study, the team genetically engineered mice with higher than usual levels of O-GlcNAc in heart muscle cells.
The animals developed severe heart failure. Their hearts began to weaken and pump less blood at just 6 weeks old. By 25 weeks of age, more than half of all mice had died, while no control animals with normal levels of O-GlcNAc had died.
Animals with lower than usual O-GlcNAc in their heart cells—remained healthy, however, and showed no signs of heart failure.
The team then found high levels of O-GlcNAc could be reversed to help prevent end-stage heart failure.
The mice no longer developed heart failure or died early when the O-GlcNAc in their heart cells were reduced.
The finding suggests that drugs targeting the O-GlcNAc pathway could help prevent heart failure.
The team says most existing heart failure therapies—including beta-blockers, diuretics and ACE inhibitors—target the same few molecular pathways.
O-GlcNAc represents a completely new pathway that hasn’t been targeted with therapeutics before, so that’s really exciting.
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The study is published in Circulation. One author of the study is Priya Umapathi, M.D.
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