- A research team led by Ching-Pin Chang, MD, PhD, at Indiana University, stopped progression of heart failure in mice by restoring levels of a specific cardiac molecule.
- The molecule is a long, non-coding RNA. This molecule's function was previously unknown.
- An article detailing Dr. Chang’s research results has been published in the latest issue of Nature.
This discovery could significantly shift drug development efforts in the area of cardiovascular (CVD) therapeutics. The molecule has been dubbed MyHeart -- short for myosin heavy-chain-associated RNA transcript. MyHeart controls BRG1 -- a protein that is critical during fetal development, but becomes dormant until stress triggers its genetic expression, leading to heart failure. When this occurs, MyHeart is suppressed.
The ultimate goal is to replace MyHeart and stop heart failure. The main challenge, however, is that MyHeart is too large of a molecule to be delivered as a drug, so Dr. Chang and his colleagues are trying to identify smaller portions of MyHeart that have the same mode of action.