Drug-induced mitochondrial dysfunction in cardiac and skeletal muscle injury

Abstract

Background: The list of clinically relevant molecules that affect skeletal and cardiac muscle mitochondria is gradually increasing, which strongly suggest that mitochondrial toxicity should be an important end point during the design and testing of novel pharmaceuticals. Objective: The present review intends to describe mechanisms by which clinically relevant drugs are known to alter mitochondrial function in cardiac and skeletal muscle, which is suggested to be involved in the toxicity associated with those drugs. Methods: Literature databases were searched in order to identify clinically relevant drugs with associated mitochondrial muscle toxicity. Conclusion: Mitochondrial function is important in the context of muscle survival, hence, the requirement to identify novel mitochondrial targets and develop new therapies to counteract chemical-induced degeneration of mitochondrial function and muscle performance.