Document Detail

Rise above: muscle ring-finger-1 (MURF1) regulation of cardiomyocyte size and energy metabolism.
MedLine Citation:
PMID:  21686210     Owner:  NLM     Status:  MEDLINE    
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.
Cam Patterson; Monte S Willis; Andrea Portbury
Publication Detail:
Type:  Journal Article    
Journal Detail:
Title:  Transactions of the American Clinical and Climatological Association     Volume:  122     ISSN:  0065-7778     ISO Abbreviation:  Trans. Am. Clin. Climatol. Assoc.     Publication Date:  2011  
Date Detail:
Created Date:  2011-06-20     Completed Date:  2011-09-30     Revised Date:  2014-04-15    
Medline Journal Info:
Nlm Unique ID:  7507559     Medline TA:  Trans Am Clin Climatol Assoc     Country:  United States    
Other Details:
Languages:  eng     Pagination:  70-81     Citation Subset:  IM    
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Adenosine Triphosphate / metabolism
Cardiomegaly / genetics,  metabolism,  pathology,  physiopathology,  prevention & control*
Cell Size*
Disease Models, Animal
Energy Metabolism*
Mice, Knockout
Mice, Transgenic
Muscle Proteins / deficiency,  genetics,  metabolism*
Myocytes, Cardiac / metabolism*,  pathology
Time Factors
Ubiquitin-Protein Ligases / deficiency,  genetics,  metabolism*
Grant Support
Reg. No./Substance:
0/Muscle Proteins; 8L70Q75FXE/Adenosine Triphosphate; EC protein, human; EC protein, mouse; EC Ligases

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

Previous Document:  Therapeutic Hypothermia: What's Hot about Cold.
Next Document:  Regulation of renal urea transport by vasopressin.