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Blood flow to the heart ceased during heart attack, this leads to death of the heart muscles, heart muscle does not regenerate; it replaces dead tissue with scars made of fibroblasts that do not pump blood to the heart.
People who had severe heart attack will develop heart failure, restoring cardiac function by reprogramming scar tissue into cardiomyocyte-like can reduce risk of heart failure.
Researchers has shown that applying a cocktail made of transcription factors Gata4, Mef2c and Tbx5 GMT results in less scar tissue, or fibrosis, and up to a fifty percent increase in cardiac function in small animal models of the disease.
This result was presumed to be mostly a consequence of the reprograming of heart fibroblasts into cardiomyocyte-like cells. They noticed that reduced fibrosis and improved cardiac function far exceeded the extent of induced new cardiomyocyte-like cells.
The research team investigated how the GMT cocktail activated mechanisms that reduced fibrosis. They discovered that of the three components in the GMT cocktail, only Gata4 was able to reduce post-heart attack fibrosis and improve cardiac function in a rat model of heart attack.
Adding Gata4 to rat fibroblasts showed an reduced expression of Snail, the master gene of fibrosis. Gata4 plays a complex role in heart regeneration: as part of the GMT cocktail, it contributes to the reprograming of fibroblasts into cardiomyocyte-like cells. It can also contributes to the development of an enlarged heart and decrease cardiac fibrosis.
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