More than 200 million people worldwide take statins to lower cholesterol and reduce their risk of heart attacks and strokes. However, some experience muscle pain, weakness, or tiredness. A small number develop severe muscle damage that can lead to kidney failure. Muscle symptoms cause some patients to stop taking their medicine, potentially leaving them without its protection against heart disease.
Researchers at the University of British Columbia and the University of Wisconsin-Madison identified a process that helps explain this damage. Using a powerful imaging method, they examined a protein called RyR1, which acts as a gate controlling calcium movement inside muscle cells. Calcium is normally released when muscles need to contract. The team focused on atorvastatin, a commonly prescribed statin. They found that three drug molecules can attach to a pocket in the protein. The first makes the closed gate more likely to open. Two more then enter and keep it open, allowing calcium to leak continuously and potentially damage muscle tissue. Other statins may interact with the protein in a similar way.
The discovery could help scientists change the parts of statin molecules that affect muscle proteins. This might reduce muscle damage while preserving the drugs’ cholesterol-lowering benefits. However, further research and drug development are needed before the findings can lead to new treatments.
