Researchers have now linked non-coding or "junk DNA" to heart failure in humans. The study, conducted by researchers at Washington University School of Medicine in St. Louis found that a large section of the human genome, which was previously dismissed as junk, is responsible for heart failure. Junk DNA is the genetic material that doesn't code for proteins and is considered insignificant in heredity and diseases. Research has shown that the non-coding region of the genome produce RNA molecules, which can affect biological processes in the body. RNA or ribonucleic acids are close cousins of DNA. Molecules associated with this region are called noncoding RNAs. A group of these RNAs called long noncoding RNAs are widely studied in medical research. The current study was conducted on eight nonfailing hearts, eight hearts in ischemic heart failure and eight hearts in nonischemic heart failure, according to a news release. The research was conducted before and after a surgery to implant left ventricular assist devices (LVAD). The LVADs reduce the heart's pumping capacity and are used in people who are waiting for heart transplants. "We took an unbiased approach to investigating which types of RNA might be linked to heart failure," said senior author Jeanne M. Nerbonne, PhD, the Alumni Endowed Professor of Molecular Biology and Pharmacology. "We were surprised to find that long noncoding RNAs stood out. In fact, the field is evolving so rapidly that when we did a slightly earlier, similar investigation in mice, we didn't even think to include long noncoding RNAs in the analysis." Heart failure is when the heart can't pump enough blood in the body. In this condition, the left ventricle, the heart's main pumping chamber, loses its efficiency. Researchers found that activity of the long noncoding RNA was different in heart failure patients in both the categories; ischemic and non-ischemic. The RNAs could also distinguish between failing hearts "We don't know whether these changes in long noncoding RNAs are a cause or an effect of heart failure," Nerbonne said. "But it seems likely they play some role in coordinating the regulation of multiple genes involved in heart function." The study is published in the journal Circulation and was funded by al Heart, Lung and Blood Institute (NHLBI) of the National Institutes of Health (NIH) and the NIH National Center for Research Resources.
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