An imbalance between the heart’s molecular motor units that get switched on and the few that remain off may contribute to excessive contraction of the heart muscle and its failure to relax normally, according to a study published in Circulation.
The study’s findings reveal that this balancing act occurs across human, mouse and squirrel heart cells to regulate heart muscle contraction and prevent gradual overexertion, thickening and failure.
When myosin, the main contractile protein of the heart muscle, goes awry, it triggers a cascade of molecular events that leads to over-exertion of the heart muscle and hypertrophic cardiomyopathy (HCM).
In subsequent experiments, researchers treated human and mouse heart cells engineered to carry gene mutations linked to HCM with an experimental drug treatment. The treatment restored the imbalance and normalized the contraction and relaxation of the cells.
Future experiments, researchers say, may inform therapies that halt disease progression and prevent complications. The study was funded by NHLBI.