Goals
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| + | The problem: 1,200,000 people suffer a (new or recurrent) MI every year, and about 40% of them die as a result of the attack. Current therapies are inadequate. Drugs at best can only stabilize the condition. Endogenous Adult Stem cells are not programmed to repair the heart. | ||
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Our goal is to repair damaged hearts. We are engineering embryonic stem-like cells to autonomously differentiate into cardiomyocytes, recognize and bind to damaged heart cells and then activate a defined program. Bound cells will express anti-apoptosis and anti-necrosis proteins to prevent cell death, express increased amounts of a cell-cell adhesion molecule to stimulate the formation of a sheet of cells and to cause some of the cells to penetrate into the inner layers of the heart. Cells will also express a growth factor to stimulate new blood vessel formation. Cells that fail to bind in a defined amount of time are programmed to self-destruct. | Our goal is to repair damaged hearts. We are engineering embryonic stem-like cells to autonomously differentiate into cardiomyocytes, recognize and bind to damaged heart cells and then activate a defined program. Bound cells will express anti-apoptosis and anti-necrosis proteins to prevent cell death, express increased amounts of a cell-cell adhesion molecule to stimulate the formation of a sheet of cells and to cause some of the cells to penetrate into the inner layers of the heart. Cells will also express a growth factor to stimulate new blood vessel formation. Cells that fail to bind in a defined amount of time are programmed to self-destruct. | ||
Revision as of 03:58, 27 October 2007
The problem: 1,200,000 people suffer a (new or recurrent) MI every year, and about 40% of them die as a result of the attack. Current therapies are inadequate. Drugs at best can only stabilize the condition. Endogenous Adult Stem cells are not programmed to repair the heart.
Our goal is to repair damaged hearts. We are engineering embryonic stem-like cells to autonomously differentiate into cardiomyocytes, recognize and bind to damaged heart cells and then activate a defined program. Bound cells will express anti-apoptosis and anti-necrosis proteins to prevent cell death, express increased amounts of a cell-cell adhesion molecule to stimulate the formation of a sheet of cells and to cause some of the cells to penetrate into the inner layers of the heart. Cells will also express a growth factor to stimulate new blood vessel formation. Cells that fail to bind in a defined amount of time are programmed to self-destruct.
