The loss of skeletal muscle function is a leading cause of frailty and loss of independence in the elderly, which comes along with significant healthcare costs. Mitochondrial dysfunction plays a key pathogenic role in aging skeletal muscle, but currently there is no pharmacologic treatment to rapidly reverse mitochondrial deficits in the elderly.
David Marcinek’s lab examines the effect of aging on mitochondrial function in skeletal muscle and their surprising new discovery may lead to a new strategy for reversing age-related deficits in skeletal muscle with potential for translation into human use.
Mitochondria play an important role in maintaining healthy skeletal muscle because they are responsible for meeting the majority of the energy demand for contraction. Mitochondria also control many aspects of cell function by generating signaling molecules called reactive oxygen species (ROS). As mitochondria age they work less efficiently and generate too much (ROS), which disrupts normal function.
Researchers in Marcinek’s lab recently made the discovery that treating aged mice with a new drug, Bendavia (SS-31) (currently in clinical trials for use in people) reduced mitochondrial ROS production and improved muscle energy metabolism and skeletal muscle performance in aged mice in as little as 1 hour.
The study results, published in the October 2013 Aging Cell article, Mitochondrial-targeted peptide rapidly improves mitochondrial energetics and skeletal muscle performance in aged mice, highlight the new perspective that age-related effects on mitochondrial function are much more dynamic and malleable that previously thought. This finding is particularly exciting says Marcinek, it “is driving our research in a new direction and opens new avenues for developing short term interventions to improve quality of life in the elderly.”
