Mark Mercola, a scientist who studies heart disease at Sanford-Burnham Medical Research Institute.

A team including Sanford-Burnham Medical Research scientists has identified a form of RNA that plays a key role in inducing heart failure.

Called miR-25, the molecule is a short fragment of RNA, called microRNA. In a model of heart failure in mice, increasing the level of miR-25 reduced the efficiency of heart muscle contraction. Inhibiting miR-25 halted heart failure that had already been established.

The study was published Wednesday in the journal Nature. (If link is not live, check later). Scientists from the Icahn School of Medicine at Mount Sinai and UC San Diego collaborated with Sanford-Burnham scientists in the study.

The microRNA molecule blocks activity of a gene called SERCA2a, which regulates the flow of calcium ions into cardiac tissue. The gene has been identified in another study as a target for gene therapy in heart failure.

In this study, led by Sanford-Burnham heart disease researcher Mark Mercola, the gene activity was boosted by using antisense technology to inactivate miR-25. Antisense RNA molecules form a complementary sequence to the specific RNA molecule, called the "sense" molecule, they inactivate. The antisense molecules bind to the targeted RNA molecules, which prevents them from serving as a template for protein production.

The culprit molecule was identified with a functional screening system developed at Sanford-Burnham Mercola said in a Sanford-Burnham press release. Mercola is a professor in the Development, Aging, and Regeneration Program at Sanford-Burnham and a professor of bioengineering at UC San Diego Jacobs School of Engineering.

"Before the availability of high-throughput functional screening, our chance of teasing apart complex biological processes involved in disease progression like heart failure was like finding a needle in a haystack," Mercola said in the press release. "The results of this study validate our approach to identifying microRNAs as potential therapeutic targets with significant clinical value."

The screen searched through all human microRNAs to find those linked to heart failure. Colleagues at the Cardiovascular Research Center at Icahn School of Medicine at Mount Sinai found that injecting the antisense complement to miR-25 stopped heart-failure progression in mice, improved cardiac function and survival.

Heart failure is a progressive loss of the heart's ability to pump blood. It can be caused by heart attacks, high blood pressure, diabetes and other conditions. As heart failure worsens, patients become increasingly restricted in their physical activities. The disease affects nearly six million Americans.

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