Resolving a Catch-22 in Cardiac Gene Regulation
"You have a big heart." These five words have almost as many implications. Being "big hearted" can describe a generous and giving nature. In a different context, Secretariat's heart was unusually large because he carried an X-linked gene1 conferring on him rare physiological attributes that in 1973 propelled him to thoroughbred horse racing's Triple Crown. When the same declaration occurs between cardiologist and patient, however, the connotation is overwhelmingly negative. Heart enlargement from cardiac hypertrophy or dilated cardiomyopathy is a powerful positive predictor of morbidity and mortality2,3. Accordingly, efforts to more fully understand the molecular underpinnings of structural and functional cardiac remodeling have been a major focus of basic cardiovascular research since genetic reprogramming was first mechanistically linked to cardiac hypertrophy4,5. Over the past 25 years major transcriptional controls for pathological cardiac gene expression have been defined and suggested novel genetic approaches to control or reverse hypertrophy6. (SELECT FULL TEXT TO CONTINUE)
- Received April 30, 2012.
- Accepted May 2, 2012.
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