Mitochondrial oxidative stress alters aged muscle function through oxidation of the thiol proteome
Loss of muscle function with age is an important public health concern due to its role in increased morbidity, loss of independence, and nursing home placement. Despite this, there are few treatment options available to improve muscle performance in the elderly. That is due in large part to a poor understanding of the mechanisms that underlie this dysfunction.
Short-term stresses, like exercise, are a normal part of physiology and play a critical role in signaling muscle to adapt to changing demands. In contrast, Dr. Marcinek is interested in how persistent stresses as associated with aging and chronic disease disrupt these normal responses and contribute to poor health.
Dr. Marcinek’s research focuses on how mitochondria, the powerhouses of the cell, affect the ability of skeletal muscle to respond to stress. His lab has found that reducing mitochondrial oxidative stress leads to improved energy use and muscle performance within one hour of treatment in aged skeletal muscles. This has led to an ongoing clinical trial and demonstrated that the interaction between mitochondrial oxidative stress and aging muscle function is more dynamic than previously thought.
Dr. Marcinek will now test a novel regulatory mechanism underlying this interaction through the reversible oxidation of muscle proteins. His research could further define the mechanisms by which manipulation of mitochondrial function can rapidly improve health in the elderly.