Scientists Finally Uncover Why the World’s Most Common Heart Drug Causes Muscle Pain . A new study explains how cholesterol-lowering medications can lead to damage and identifies a possible approach to making these treatments safer.
Statins have dramatically improved cardiovascular health by lowering cholesterol levels and reducing the likelihood of heart attacks and strokes. Yet many people who take these medications experience unwanted muscle symptoms, including soreness, weakness, and in rare situations, severe muscle breakdown that can harm the kidneys.
Researchers have now uncovered the biological reason behind these side effects. Their results, published last week in Nature Communications, may help guide the development of statins that do not trigger muscle problems.
Using cryo-electron microscopy, a technique capable of visualizing proteins at extremely high resolution, the team observed how statins interact with a key muscle protein known as the ryanodine receptor (RyR1). This receptor controls the flow of calcium inside cells and opens only when a it is meant to contract. When statins attach to it, however, the channel is forced open, causing calcium to escape continuously, which can injure the surrounding muscle fibers.
“We were able to see, almost atom by atom, how statins latch onto this channel,” said lead author Dr. Steven Molinarolo, a postdoctoral researcher in UBC’s department of biochemistry and molecular biology. “That leak of calcium explains why some patients experience muscle pain or, in extreme cases, life-threatening complications.”
How statins bind to the calcium channel
The study examined atorvastatin, one of the most commonly used statins, but the evidence suggests the same effect could occur with other drugs in this class. The researchers found that three statin molecules gather within a single pocket of the protein. The first molecule connects when the channel is closed, preparing it to open, while the other two settle in afterward and push the channel fully open.
