The redox environment and mitochondrial dysfunction in age-related skeletal muscle atrophy

Medical advancements have extended human life expectancy, which is not always accompanied by an improved quality of life or healthspan. A decline in muscle mass and function is a consequence of ageing and can result in a loss of independence in elderly individuals while increasing their risk of falls. Multiple cellular pathways have been implicated in age-related muscle atrophy, including the contribution of reactive oxygen species (ROS) and disrupted redox signalling. Aberrant levels of ROS disrupts the redox environment in older muscle, potentially disrupting cellular signalling and in some cases blunting the adaptive response to exercise. Age-related muscle atrophy is associated with disrupted mitochondrial content and function, one of the hallmarks of age-related diseases. There is a critical link between abnormal ROS generation and dysfunctional mitochondrial dynamics including mitochondrial biogenesis, fusion and fission. In order to develop effective treatments or preventative strategies, it is important to gain a comprehensive understanding of the mechanistic pathways implicated in age associated loss of muscle.