In a major discovery that may eventually help scientists treat heart problems that kill millions of people every year, scientists have identified how a particular protein plays a central role in the continuous heartbeat. Those beats must be precisely calibrated; even a small divergence from the metronomic rhythm can cause sudden death.
Researchers have for the first time described how myosin-binding protein C (“C protein”) allows the muscle fibers in the heart to work in perfect synchrony. “This protein turns out to be really important to this process,” said W. Jonathan Lederer, professor of physiology at the University of Maryland School of Medicine.
Researchers have known that calcium acts as a trigger for the heartbeat, activating proteins that cause the sarcomeres – the fibrous proteins that make up heart muscle cells – to contract. The calcium molecules are not distributed evenly across the length of each sarcomere; the molecules are released from the ends.
Despite this, the sarcomeres contract uniformly but the process was a mystery. Now the researchers have found the answer in C protein. Using an animal model, the researchers studied the physiology of sarcomeres, measuring calcium release and the muscle fibers’ mechanical reaction.It turns out that C protein sensitises certain parts of the sarcomere to calcium.
As a result, the middle of the sarcomere contracts just as much as the ends, despite having much less calcium. In fact, C protein enables the sarcomeres to contract synchronously. “Calcium is like the sparkplugs in an automobile engine and C protein acts like the rings that increase the efficiency of the movement of the pistons,” said Michael J. Previs, assistant professor at the University of Vermont.
C protein appears to play a large part in many forms of heart disease. Defects in C-protein may lead to extremely serious arrhythmias, which cause sudden death when the heart loses the ability to pump blood. “Beyond the elegant findings of this work, there remain many challenges in unravelling how C protein mutations produce contractile and arrhythmic dysfunction in disease,” concluded said Dean E. Albert Reece from the University of Maryland. The results appeared in the journal Science Advances. (IANS)