UBC team reveals how statins trigger muscle damage — SkimNews

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- UBC researchers used cryo-electron microscopy to show that statins attach to the ryanodine receptor (RyR1) in muscle cells, forcing open a channel that normally controls calcium flow and causing continuous leakage that can damage tissue.
- Structural imaging revealed a sequential mechanism: the first statin molecule binds while the channel is closed, making it more likely to open, then two additional molecules enter the same pocket and hold the channel open.
- Lead author Dr. Steven Molinarolo, a postdoctoral researcher in UBC's biochemistry department, said the team could see "almost atom by atom" how statins latch onto the channel and that the calcium leak "explains why some patients experience muscle pain or, in extreme cases, life-threatening complications."
- The study, published in Nature Communications and conducted with the University of Wisconsin-Madison, focused on atorvastatin but found that the researchers expect similar interactions with other medications in the statin family.
- Senior author Dr. Filip Van Petegem of UBC's Life Sciences Institute called it "the first time we've had a clear picture of how statins activate this channel" and said the finding offers "a roadmap for designing statins that don't interact with muscle tissue."
- More than 200 million people worldwide take statins, and while severe muscle injury is rare, widespread but milder effects like soreness, weakness, and fatigue cause some patients to discontinue medication and lose cardiovascular protection.
Why it matters: Roughly 200 million people take statins, and muscle-related side effects are common enough that some users stop their medication and lose cardiovascular protection; the UBC team has now mapped the exact protein interaction behind those symptoms, giving drug developers a concrete structural target for designing next-generation statins that preserve cholesterol-lowering benefits while eliminating muscle damage at its molecular source.
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