Researchers from the Massachusetts General Hospital (MGH) have shown that it is possible to improve cardiac function in aging rats by delivering extra copies of a key gene to the heart muscle via gene therapy techniques. In the Feb. 22 issue of Circulation the team reports that transferring additional copies of the gene SERCA2a directly into the hearts of aging rats alleviated a typical functional abnormality of aging hearts called diastolic dysfunction, an inability of the heart muscle to relax normally. Previous research in animals and in human heart muscle cells has shown that increasing SERCA2a could improve the function in actual heart failure, but this study is the first to show that altering gene expression could improve the more common heart abnormalities associated with normal aging.
"As our population continues to age in the coming years, we know we're going to be seeing more and more people with heart failure, which already is the most frequent cause of hospitalization in people over 65 in this country," says Roger Hajjar, MD, of the MGH Cardiovascular Research Center (CVRC), the paper's senior author. "The knowledge that increasing SERCA2a gene expression might improve function of the aging heart gives us a target for therapies that might prevent people from progressing to heart failure."
Hajjar adds that such therapies could be based on new medications that might impact the process controlled by SERCA2a or could utilize new gene therapy approaches with delivery vectors, some currently in development, that promise to be more effective and safer than the adenovirus-based system used in this study. He also stresses that it is by no means certain that these animal results will carry over to human patients and that additional research is required to verify and follow up the current findings.
In congestive heart failure the heart muscle is weakened and cannot pump effectively, allowing fluids to back up in the circulatory system and som
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Contact: Susan McGreevey
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617-724-2764
Massachusetts General Hospital
21-Feb-2000