Rise above

muscle ring-finger-1 (MURF1) regulation of cardiomyocyte size and energy metabolism.

Cam Patterson, Monte Willis, Andrea Portbury

Research output: Contribution to journalArticle

3 Citations (Scopus)

Abstract

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 languageEnglish (US)
Pages (from-to)70-81
Number of pages12
JournalTransactions of the American Clinical and Climatological Association
Volume122
StatePublished - Oct 4 2011
Externally publishedYes

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Cardiomegaly
Cardiac Myocytes
Energy Metabolism
Fingers
Muscles
Heart Failure
Phosphocreatine
Ligases
Ubiquitin
Transgenic Mice
Cause of Death
Fatty Acids
Hypertension
Glucose

ASJC Scopus subject areas

  • Medicine(all)

Cite this

Rise above : muscle ring-finger-1 (MURF1) regulation of cardiomyocyte size and energy metabolism. / Patterson, Cam; Willis, Monte; Portbury, Andrea.

In: Transactions of the American Clinical and Climatological Association, Vol. 122, 04.10.2011, p. 70-81.

Research output: Contribution to journalArticle

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