Agencies
... Read More
By clicking “Accept All Cookies”, you agree to the storing of cookies on your device to enhance site navigation, analyze site usage, and assist in our marketing efforts. Cookie Policy.
Written By: Agencies | Published : March 14, 2014 12:31 PM IST
In a major medical breakthrough, researchers have identified the main component that is responsible for the onset and progression of heart failure. The study, conducted by Sanford-Burnham Medical Research Institute, the Cardiovascular Research Center and the University of California, also shows how they successfully blocked the newly discovered culprit to halt the debilitating and chronic life-threatening condition in its tracks. (Read: Should India have separate guidelines for preventing heart diseases?)
In the study, investigators identified a tiny piece of RNA called miR-25 that blocks a gene known as SERCA2a, which regulates the flow of calcium in and out of heart-muscle cells. Decreased SERCA2a activity is one of the main causes of poor contraction of the heart and enlargement of heart-muscle cells leading to heart failure. (Read: Natural remedies for heart disease (Gallery))
Using a functional screening system developed by researchers at Sanford-Burnham, the research team discovered miR-25 acts pathologically in patients suffering from heart failure, delaying proper calcium uptake in heart-muscle cells. Subsequently, the researchers at the Cardiovascular Research Center at Icahn School of Medicine found that injecting a small piece of RNA to inhibit the effects of miR-25 dramatically halted heart-failure progression in mice. In addition, it also improved their cardiac function and survival. The study is published in the journal Nature. (Read: Stave off heart disease, eat fibre rich foods)
Source: ANI
For more articles on heart disease , visit our heart disease section. Follow us on Facebook and Twitter for all the latest updates! For daily free health tips, sign up for our newsletter. And to join discussions on health topics of your choice, visit our forum.
