Molecular Mechanisms and Current Treatment Strategy of Sarcopenia and Cachexia

Dear Colleagues,

Skeletal muscle is the most abundant tissue in the body, comprising 40–50% of body mass and playing vital roles in locomotion, heat production during periods of cold stress, and overall metabolism. That skeletal muscle consists of the largest pool of proteins in the whole organism, which highlights why this specific tissue is highly sensitive under conditions that act to alter the balance between protein synthesis and degradation.

Two common but distinct conditions characterized by a loss of skeletal muscle mass are sarcopenia and cachexia. Muscle wasting is an inevitable part of aging (sarcopenia). Cachexia is associated not only with chronic diseases, most commonly cancer, but also with other inflammatory conditions, such as chronic obstructive pulmonary disease (COPD), heart failure, chronic kidney disease, AIDS, and sepsis.

Sarcopenia and cachexia occur due to a multifactorial process that involves physical activity, nutritional intake, metabolic homeostasis, oxidative stress, hormonal changes, and life span. The specific contribution of each of these factors is unknown, but more recent studies have indicated an apparent functional defect in autophagy-dependent signaling in both sarcopenic and cachectic muscles. In contrast, many investigators have failed to demonstrate age-related enhancement in the ubiquitin-proteasome system in the case of sarcopenia. Since many researchers try to elucidate the molecular mechanism of sarcopenia and cachexia, recent understanding is very broad.

A recent review indicated the effectiveness of exercise training and some hormonal, nutritional, and pharmacological approaches for these two conditions. In addition, sarcopenia has been most attenuated by mild caloric restriction (CR) in all mammals. In contrast, treatment with ghrelin is well known to exhibit positive effects on cancer cachexia.

This Topical Collection aims to provides recent research advances dealing with molecular mediators modulating muscle mass in both sarcopenia and cachexia. In addition, this topic includes recent attenuating strategies (hormone, pharmacology, nutrition, etc.) for this wasting.

We look forward to your contributions.

Prof. Dr. Kunihiro Sakuma
Collection Editor

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