New-look heart failure treatment shows early promise
Reducing the activity of a specific protein, RBM20, may provide significant relief for certain patients with heart failure, particularly those with preserved ejection fraction (HFpEF), according to a new analysis published in Cardiovascular Research.[1]
HFpEF is associated with stiff, rigid cardiac muscles. A team of researchers out of the University of Missouri School of Medicine believe they may be able to improve HFpEF symptoms by limiting RBM20’s influence in the heart and encouraging another protein, titin, to thrive.
“Titin is a protein found in cardiac muscle cells and acts as a ‘spring,’ enabling the heart chamber to recoil and stretch sufficiently,” lead author Mei Methawasin, MD, PhD, said in a statement. “In HFpEF, it’s common for the titin to stiffen and no longer be as flexible. We learned that if we reduced the activity of a different protein, RBM20, it caused longer and more flexible filaments of titin and significantly improved heart filling in mice.”
There are certain risks associated with too much RBM20 inhibition. Methawasin emphasized that it would be critical to find the “right balance” and not taking things too far.
“In this study, our team targeted a 50% reduction in activity, a level we chose based on our previous research,” she said. “We believe the exact decrease could be adjusted according to the severity of the patient’s heart failure.”
Additional research is still necessary—clinical trials on humans, for example—but this new approach to treating HFpEF could be a potential game-changer for high-risk heart patients.
“By restoring the heart’s most fundamental function, we hope to help individuals with heart failure enjoy an improved quality of life and more time with their loved ones,” Methawasin said.
Click here for the full analysis.
Michael has more than 19 years of experience as a professional writer and editor. He has written at length about cardiology, radiology, artificial intelligence and other key healthcare topics.