Anti-cancer agent promotes heart tissue regeneration

The heart does not continuously renew throughout life.

Update: 2017-02-04 06:33 GMT
Because of the heart's inability to repair itself, damage caused by a heart attack causes permanent scarring. (Photo: Pixabay)

Dallas: In a latest development, researchers have found out that cancer drug could promote regeneration of heart tissue.

An anticancer agent in development promotes regeneration of damaged heart muscle 0- an unexpected research finding that may help prevent congestive heart failure in the future. The study findings were published online this week in Proceedings of the National Academy of Sciences.

Many parts of the body, such as blood cells and the lining of the gut, continuously renew throughout life. Others, such as the heart, do not. Because of the heart's inability to repair itself, damage caused by a heart attack causes permanent scarring that frequently results in serious weakening of the heart, known as heart failure.

For years, Dr. Lawrence Lum, Associate Professor of Cell Biology at UT Southwestern Medical Center, has worked to develop a cancer drug targeting Wnt signaling molecules. These molecules are crucial for tissue regeneration, but also frequently contribute to cancer. Essential to the production of Wnt proteins in humans is the porcupine (Porcn) enzyme, so-named because fruit fly embryos lacking this gene resemble a porcupine. In testing the porcupine inhibitor researchers developed, they noted a curiosity.

"We saw many predictable adverse effects -0 in bone and hair, for example 0- but one surprise was that the number of dividing cardiomyocytes (heart muscle cells) was slightly increased," said Dr. Lum, senior author of the paper, and a member of UTSW's Hamon Center for Regenerative Science and Medicine. "In addition to the intense interest in porcupine inhibitors as anticancer agents, this research shows that such agents could be useful in regenerative medicine."

Based on their initial results, the researchers induced heart attacks in mice and then treated them with a porcupine inhibitor. Their hearts' ability to pump blood improved by nearly twofold compared to untreated animals.

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