Possible Therapeutic Use for a Cardiac RNA Fragment

This mouse population was then exposed to various chemical or physical stress factors, and the subsequent effect on the animals' hearts was determined. Results published in the March 22, 2007, online edition of Science Express revealed that the engineered mice lacking miR-208 maintained normal heart morphology with low levels of beta-MHC. This was in contrast to normal mice exposed to the same stress factors that suffered heart damage and increased beta-MHC production.

"We have discovered a new and completely unanticipated mechanism for regulating the contractility of the heart,” said senior author Dr. Eric Olson, professor of molecular biology at the University of Texas Southwestern Medical Center. "We are very excited about the therapeutic implications, but we still have much work left to do. Although miR-208 appears to damage the heart during stress, it may have beneficial functions for maintaining normal action of heart muscle cells. So any therapeutic approach would probably need to target its harmful stress responses while leaving normal function alone.”


Related Links:
University of Texas Southwestern Medical Center