Skeletal Muscle Homeostasis and Aging in Drosophila

Abstract

A debilitating feature of aging in humans is the progressive loss of skeletal muscle mass and function termed sarcopenia. A variety of intrinsic and extrinsic factors that are induced by aging contribute to sarcopenia, which in turn is a risk factor for many other age-related diseases. While widely studied in human and rodent models, sarcopenia has been identified also in the common fruit fly Drosophila melanogaster. Drosophila is emerging as a powerful system to study the mechanisms underlying sarcopenia, as it shares many of the same skeletal muscle characteristics as mammalian models. Decreased protein homeostasis, mitochondrial dysfunction, increased apoptosis, and alterations in transcription are just a few of the features of sarcopenia that are shared between mammals and Drosophila. Given its short life span compared to mammals and the ease in conducting genetic manipulations, including genome-wide muscle-specific transgenic screens, Drosophila offers unique advantages for studying the fundamental mechanisms of skeletal muscle aging and may provide potential therapeutic targets to combat sarcopenia in humans.