Role of nerve-muscle interactions and ROS in regulation of muscle proteostasis with aging

Abstract

Skeletal muscle aging is characterised by atrophy, a deficit in specific force generation, increased susceptibility to injury, and incomplete recovery after severe damage. The hypothesis that increased generation of Reactive Oxygen Species (ROS) in vivo plays a key role in the aging process has been extensively studied, but remains controversial. Skeletal muscle generates ROS at rest and during exercise. ROS can cause oxidative damage particularly to proteins. Indeed, products of oxidative damage accumulate in skeletal muscle during aging and the ability of muscle cells to respond to increased ROS becomes defective. The aim of this review is to examine the evidence that ROS manipulation in peripheral nerves and/or muscle modifies proteostasis mechanisms in skeletal muscle and plays a key role in initiating sarcopenia.

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