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Over the last decades, a large body of literature helped characterize the process, defining the disruptive muscle phenotype caused by COPD that involves reduction in muscle mass, force-generation capacity, fatigue-tolerance, and regenerative potential following injury. A major limitation in the field has been the scarcity of well-calibrated animal models to conduct mechanistic research based on loss- and gain-of-function studies. This article provides an overall description of the process, the tools available to mechanistically investigate it, and the potential role of mitochondrially driven metabolic signals on the regulation muscle regeneration after injury in COPD. 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