Can a protein called caveolin-3 reveal a new way to treat heart failure?

The role of caveolin-3 in cardiac myocyte structure and function

A regular and synchronised heartbeat is crucial for the heart to pump blood efficiently around the body. Levels of calcium must rapidly increase in a synchronised way in every heart cell to enable the heart to contract. Folds or ‘invaginations’ on the surface of heart cells called transverse (t-) tubules enable the calcium rise to be rapid and regular. In heart failure, this calcium rise is much slower than normal. Professor Clive Orchard from the University of Bristol has discovered that other key proteins that convert the electrical signal that a heart cell receives into a contraction are also located by the t-tubule. T-tubules do not develop until the first few weeks of life, and their structure and density is altered in heart failure. But we do not know how they form or are maintained during development, ageing or heart failure, or how the other key proteins come to be located in there. Problems with these processes may prevent heart cells from working properly. Professor Orchard believes a protein called caveolin-3 (Cav-3) is responsible for enabling t-tubules to form and for their specialised role in calcium handling. The BHF has awarded him a grant to determine whether altering levels of Cav-3 influences how t-tubules form and how they work, and whether it affects the proteins located within them. In mice, he will find out if changes to t-tubules that occur by altering Cav-3 ultimately influence how heart cells work and contract, in both health and disease. He will also investigate whether increasing the amount of Cav-3 can stop or reverse changes seen in conditions such as heart failure. This research will reveal more about the intricate detail of heart cell contraction necessary for our hearts to beat efficiently and effectively. It may reveal new ways to treat heart failure in the future.