Newswise — MAYWOOD, Ill. (June 24, 2014) – Loyola University Chicago recently hosted a meeting of more than 60 of the world’s leading researchers of a protein that could hold the key to new treatments for heart disease.
The protein, myosin binding protein C (MyBP-C), is critical for the normal functioning of striated muscles, including heart muscles. During a heart attack, cardiac isoform of MyBP-C breaks into pieces. This fragmentation coincides with myocardial damage and heart failure.
The conference was organized by Sakthivel Sadayappan, PhD, who has spent more than 15 years studying MyBP-C, and has published groundbreaking studies on the protein. Sadayappan is an associate professor in Loyola’s Department of Cell and Molecular Physiology.
Sadayappan said that understanding what happens to MyBP-C during heart failure could lead to the development of drugs to protect MyBP-C following a heart attack, and thereby limit damage to heart muscle.
After a heart attack, MyBP-C is released to the bloodstream by dying heart muscle. Sadayappan has shown that a blood test for MyBP-C could detect heart attacks hours faster than the current gold-standard blood test.
Researchers Roger Star and Gerald Offer discovered MyBP-C in 1971. However, the exact role of MyBP-C in striated muscles is not fully understood. “Given that genetic defects in this protein have been linked to familial hypertrophic cardiomyopathy and heart failure in more than 60 million people worldwide, it is clinically urgent to fully elucidate the function of MyBP-C,” Sadayappan said.
The conference was titled “Myosin Binding Protein C: Past, Present and Future.” The one-day meeting, held June, 6, 2014, provided a platform for discussing various aspects of MyBP-C, exchanging ideas, resolving controversies, networking and recognizing key scientists in the MyBP field.
"Our long-term goal is to delineate the roles of MyBP-C protein function in the heart," Sadayappan said. “This conference, which was extremely productive, will bring us closer to reaching this goal.”