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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. Now, researchers at Johns Hopkins Medicine have found evidence in mouse experiments that these excess sugars could well be a cause, not merely a consequence or marker of heart failure.
Their research found that elevated levels of O-GlcNAc made mice more prone to heart failure, but lowering levels of O-GlcNAc restored the animals risk of death and heart function to normal. Together, the investigators say, the new findings, described online in the April 27th issue of the journal