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Scientists modified a protein in the heart which dramaticallyreduced cell damage after heart attacks , according to new research published the American HeartAssociation journal Arteriosclerosis, Thrombosis and Vascular Biology. The modified protein reduced cell damage by 50 percent in micewithout causing harmful inflammation, the researchers found. Thoseresults came during research looking at ways to prevent heart failure induced by heart attack. The protein is called focal adhesion kinase, or FAK. It organizescell structure by activating various processes that help the cellsstay alive. "FAK is important for basic processes in all cells, and it appearsto be important for cell survival, growth and migration in a numberof cell types, but is especially critical in the heart," said JoanTaylor, Ph.D., who has been studying FAK in mice at the Departmentof Pathology and Lab Medicine at the University of North Carolina. FAK can create problems, too. In earlier research, the scientistsfound that it was activated in the heart after a heart attack, andspurred a series of events that could lead to inflammation andpermanent heart damage. "Inflammation is important to get rid of dead cells, but if thatgoes uncontrolled, the inflammation kills viable heart cells,"Taylor said. That's when the researchers began working to build a better FAK,one that would initiate the survival response without causingexcessive inflammation. Taylor's former University of NorthCarolina colleague, Mike Schaller, Ph.D., created what they calledSuperFAK, which exhibited increased but controlled activity. In mice with the new SuperFAK gene, researchers saw a massiveactivation of FAK after heart attack, and not as many heart cellsdied compared to unaltered mice. Three days after the induced heartattack, the SuperFAK mice had about 50 percent less heart injurythan the unaltered mice. This benefit was maintained for eightweeks. "We think because the modified FAK resolved its activity in 24hours, it limited the inflammation response, and only activatedbeneficial signals," Taylor said. FAK also plays a role in the development of a number of cancers and has been linked to tumor growth and metastases. Somechemotherapies hamper FAK, leaving the heart vulnerable.Progressive cardiac damage is a common adverse effect of severalchemotherapeutic treatments. In the future, they hope to developdrugs to target FAK to protect the heart during chemotherapy orfollowing a heart attack. Additional References Citations. I am an expert from cnc-machiningparts.com, while we provides the quality product, such as China Aluminum Die Castings , Sand Castings Manufacturer, CNC Precision Machining,and more.
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