TRPC6 Is Big Hearted

Main Category: Cardiovascular / Cardiology
Also Included In: Hypertension;  Genetics
Article Date: 14 Nov 2006 - 14:00 PST

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The causes of heart failure are extremely diverse and include high blood pressure, a heart attack, and inherited genetic abnormalities. Two of the reasons these events all trigger heart failure is that they result in the muscle cells of the heart getting bigger (a process known as cardiac hypertrophy) and they cause the muscle cells to change the types of protein they express (and so change their functions). Understanding the molecular mechanisms behind these changes is therefore of interest for developing new therapeutics for the treatment of individuals with heart disease.

Now, in a study which appeared online on November 9, in advance of publication in the December print issue of the Journal of Clinical Investigation, Eric Olsen and colleagues from the University of Texas Southwestern Medical Center have shown that in mice, increased expression of a protein known as TRPC6 is important for the muscle cells of the heart to grow and change their function under conditions that trigger heart failure. Upregulation of TRPC6 was mediated by a calcium responsive signaling molecule (calcineurin) and overexpression of TRPC6 in the heart caused mice to be more susceptible to lethal heart failure. As TRPC6 was also shown to be expressed at high levels in failing human hearts, the authors suggest that TRPC6 might be a viable therapeutic target for the treatment of heart failure.

TITLE: TRPC6 fulfills a calcineurin signaling circuit during pathologic cardiac remodeling

AUTHOR CONTACT:

Eric N. Olsen
University of Texas Southwestern Medical Center, Dallas, Texas, USA.

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JCI table of contents: November 9, 2006

Contact: Karen Honey
Journal of Clinical Investigation

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