Oxidative stress, molecular inflammation and sarcopenia

Abstract

Sarcopenia is the decline of muscle mass and strength with age. Evidence suggests that oxidative stress and molecular inflammation play important roles in age-related muscle atrophy. The two factors may interfere with the balance between protein synthesis and breakdown, cause mitochondrial dysfunction, and induce apoptosis. The purpose of this review is to discuss some of the major signaling pathways that are activated or inactivated during the oxidative stress and molecular inflammation seen in aged skeletal muscle. Combined interventions that may be required to reverse sarcopenia, such as exercise, caloric restriction, and nutrition, will also be discussed.

Keywords: chronic inflammation; interventions; oxidative stress; sarcopenia; signaling.

Figure 1.

A schematic summary of proposed mechanisms by which oxidative stress and chronic inflammation could contribute to sarcopenia. Some major signaling pathways are activated or inactivated during the oxidative stress and chronic inflammation seen in aged skeletal muscle. The pathways are related to an imbalance of protein synthesis and breakdown, mitochondrial dysfunction, and apoptosis, leading to fiber atrophy and fiber loss, eventually to sarcopenia.

Figure 2.

Hypothetical scheme for how combined interventions can affect sarcopenia.