From Our 2007 Archives

Sick Hearts Switch on a Fetal Gene

MONDAY, Feb. 19 (HealthDay News) -- U.S. researchers have identified a fetal heart-cell enzyme that they believe plays a role in the onset of heart failure in adults.

According to a team at the University of Pennsylvania School of Medicine, the enzyme, HDAC, is associated with a condition called cardiac hypertrophy (enlargement of heart cells) that's a precursor to many forms of congestive heart failure.

It has long been known that in nearly all types of heart failure, the heart starts to express genes that are normally only expressed during the fetal stage. But it has been unclear what regulates this reactivation of fetal genes in the heart.

"It's as if old programs are being reactivated in a sick heart. In an adult heart, stresses such as high blood pressure induce the re-expression of a fetal gene program," study senior author Dr. Jonathan A. Epstein, the W.W. Smith Endowed Chair for Cardiovascular Research at Penn, said in a prepared statement.

In adult mice, inhibiting HDAC prevented the fetal gene program from restarting, the study found.

Epstein and his colleagues also discovered that HDAC works in the heart, in part, by regulating expression of an enzyme called Inpp5f, which plays a role in cell growth and multiplication.

The findings, published online in the journal Nature Medicine, offer new targets for treating cardiac hypertrophy and heart failure, Epstein said.

-- Robert Preidt

SOURCE: University of Pennsylvania School of Medicine, news release, Feb. 18, 2007

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