Metabolic and contractile dysfunctions in skeletal and cardiac muscles are present in several conditions that become more prevalent with aging (e.g., sarcopenia, cardiovascular diseases, cancer, obesity and diabetes) reducing quality of life and increasing mortality. Impaired proteostasis leading to reduced proteome quality is a common feature of these conditions contributing to cellular dysfunction. Although our understanding of the different processes involved in the maintenance of proteostasis continues to evolve, the coordinated regulation of these mechanisms in contractile tissues remains poorly understood. Our overall research goal is to determine the cellular and molecular mechanisms that become compromised in these conditions thereby identifying novel targets for therapy. Deciphering the intracellular and cross-tissue pathways responsible for the exercise-mediated improvement of the skeletal and cardiac muscle proteomes is also of major interest. We conduct functional studies combining unbiased approaches (e.g., proteomics, metabolomics) with molecular biology and mouse genetics.