WIKIMEDIA, RAMADuring chronic heart failure, the muscles of the vital organ slowly lose their ability to contract. Blocking the action of microRNA-25 (miR-25)—a noncoding RNA molecule that regulates gene expression—helps restore contractility to cardiac muscles in a mouse model of chronic heart failure, according to a paper published today (March 12) in Nature. The researchers hypothesize that miR-25 exacerbates heart failure by binding and preventing translation of the mRNA that encodes the calcium pump SERCA2a, a protein that is key to heart muscle contraction. The flow of calcium in and out of the cytosol of heart muscle cells helps regulate the rhythmic muscle contractions that cause the heart to beat.
Study coauthor Mark Mercola, a cardiology researcher at the Sanford-Burnham Medical Research Institute in La Jolla, California, said there is reason to hope the path to the clinic will be smooth for the RNA-based therapeutic approach his team presents. A Phase 2 clinical trial has already demonstrated that boosting SERCA2a in human hearts via gene therapy can slow progression of chronic heart failure. “From a pharmaceutical standpoint, we have a clinically validated target,” Mercola said.
“These experiments are very interesting and exciting,” Stefanie Dimmeler, director of the Institute of Cardiovascular Regeneration at Goethe University Frankfurt in Germany, wrote in an e-mail to The Scientist. Dimmeler was not involved in the study. “SERCA2a is a very important target for treating heart failure and its augmentation by ...
