The Azerbaijan State News Agency

Researchers "Mend a Broken Heart" With Transformed Scar Tissue

Baku, August 26 (AZERTAC). Researchers are describing that the human body is much more strange and pliable than previously thought -- and that's a good thing. A shining example is the work of Professor Deepak Srivastava, MD, a professor at the Univ. of California - San Francisco (UCSF) and its affiliate Gladstone Institute labs. Dr. Srivastava first discovered that a cocktail of three genes injected into mice could provoke fibroblast cells to become cardiomyocytes -- the cells that pump blood in a beating heart. Now his team has managed to use a slightly more advanced formulation to get human fibroblasts to do the same thing.

Repairing a (literally) broken heart is one attractive target: every year nearly 600,000 Americans die of heart disease. Heart disease is the number one killer in the U.S., according to the latest statistics from the U.S. Centers for Disease Control and Prevention. It accounts for nearly 600,000 deaths in the U.S. a year, or just under 1 in 4 deaths.

The research team began by injecting all candidate genes into the human fibroblasts. They then systematically removed each one to see which were necessary for reprogramming, and which were dispensable. In the end, the team found that injecting a cocktail of five genes -- the 3-gene GMT mix plus the genes ESRRG and MESP1 -- were sufficient to reprogram the fibroblasts into heart-like cells. They then found that with the addition of two more genes, called MYOCD and ZFPM2, the transformation was even more complete. To help things along, the team initiated a chemical reaction known as the TGF-ß signaling pathway during the early stages of reprogramming, which further improved reprogramming success rates. In a healthy individual these special helper cells are like the gardeners of the regal estate that is the human heart. They maintain the collagen and other biopolymers found in the extracellular matrix, keep the heart elastic and receptive to electrical signals from the "pacemaker" -- the sinoatrial (SA) node. They also play a key role in a damaged heart, depositing scar tissue. While this may save the heart from infection and internal bleeding, it also thickens the heart and prevents it from fully healing, over time leading to death.

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