The discovery of a protein that regulates degradation of the key myocardial protein troponin may enable researchers to develop a strategy to prevent cardiac hypertrophy and diastolic heart failure, according to an article in the December 28th issue of the Proceedings of the National Academy of Science (USA).

The protein is known by the acronym MuRF1, or muscle-specific RING finger 1, and it helps regulate cardiac cellular molecules involved in cardiac hypertrophy, which occurs in 50 percent to 60 percent of people older than age 70 and makes them more vulnerable to developing diastolic heart failure. Specifically, it triggers the pathway for degradation of troponin-1.

When heart cells hypertrophy, or become enlarged, troponin-1 and other contractile proteins greatly increase in abundance, Cam Patterson, MD, senior author, said. "And so one of the critical ways that MuRF1 reverses hypertrophy is by degrading proteins such as troponin-1."

Thus, the action of MuRF1 appears to determine the balance between hypertrophic (enlargement) and anti-hypertrophic signals in heart muscle cells, Patterson added. "This is really a fundamental observation. It has been known for some time that contractile proteins are degraded, but the specific molecules involved have not been defined until now."

Cardiologists consider cardiac hypertrophy as one of the most potent predictors for adverse cardiac outcomes, such as heart failure and arrhythmias, or abnormal heart rhythms. "It's as bad to have cardiac hypertrophy as it is to have had a heart attack," said Patterson.

"Unfortunately, we have no specific therapies aimed at this condition. But our findings suggest that new drugs might be developed to reverse hypertrophy by targeting these ubiquitin ligase signaling pathways in cardiac cells."