Cardiac hypertrophy develops in response to increases in afterload, most commonly as the result of hypertension. When left untreated, cardiac hypertrophy commonly progresses to heart failure, one of the leading causes of death in the US. A number of studies have shown that reversing cardiac hypertrophy can decrease the progression to heart failure. However, the treatments now used to decrease cardiac hypertrophy have had limited success. Our laboratory has found that the novel muscle-specific ubiquitin ligase named muscle ring-finger-1 (MuRF1) inhibits cardiac hypertrophy and is necessary for its experimental reversal. We have developed transgenic mouse models that have been instrumental in unraveling some of the mechanisms by which MuRF1 inhibits cardiac hypertrophy. We have also identified specific ways in which MuRF1 regulates metabolism at the level of the phosphocreatine shuttle and fatty-acid and glucose metabolism. The knowledge gained from these studies has helped us to understand the processes regulating cardiac hypertrophy, and to identify specific pathways against which to target new therapies that can halt the progression and even possibly reverse the damage associated with cardiac hypertrophy.
|Original language||English (US)|
|Number of pages||12|
|Journal||Transactions of the American Clinical and Climatological Association|
|State||Published - Oct 4 2011|
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