JCI table of contents: September 21, 2006


CARDIOLOGY: MITF finds a new job in the heart

The heart is able to respond to its surroundings; so, if more power is needed to pump the blood around the body, for example in individuals with high blood pressure, it can increase the size of the muscle cells of the heart (a process known as cardiac hypertrophy). Now, in a study appearing online on September 21 in advance of publication in the October print issue of the Journal of Clinical Investigation, researchers from Hebrew University, Israel, have found that mice lacking a fully functional form of the protein MITF have smaller hearts than normal mice and that they are at increased risk of death in situations when the heart should respond by increasing the size of its muscle cells.

Although MITF was known to be expressed in the heart, its function there had not been previously studied. So, Ehud Razin and colleagues analyzed the hearts of mice lacking functional MITF. When mice of similar weights, which should have similar sized hearts, were compared, the mice lacking functional MITF had smaller hearts than normal mice. This inability to increase the size of the heart during development was also seen in situations that require a rapid cardiac hypertrophy response, and mice lacking MITF were more susceptible to death in these situations. This study identifies MITF as a regulator of both normal cardiac development and cardiac hypertrophy, but further work will be needed to understand how MITF is controlled during these two distinct processes.

TITLE: Transcription factor MITF regulates cardiac growth and hypertrophy

AUTHOR CONTACT: Ehud Razin Hebrew University Medical School, Jerusalem, Israel. Phone: +972-2-675-8288 Fax: +972-2-675-8986; E-mail: ehudr@cc.huji.ac.il.

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Contact: Karen Honey
Journal of Clinical Investigation

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