Skeletal muscle is a specialized contractile tissue with crucial roles in the regulation of systemic energy homeostasis. In particular, skeletal muscle is the most important site for glucose metabolism and for fatty acid oxidation. Along this line, it is considered a reservoir of amino acids that can be released as needed, supporting protein synthesis and energy production in the organism. Interestingly, skeletal muscle can adapt its metabolic role in response to physiological and pathological conditions. Several diseases, such as cancer/immune disorders/muscular dystrophies, are characterized by an increased level of cytokines, which induce chronic inflammation in the organism. This condition causes a reduction in protein synthesis and an enhancement in catabolism in muscle tissue, affecting energy balance and leading to the onset of cachexia.
During the last decades, several studies demonstrated that inflammation plays a crucial role in controlling metabolism in patients affected by cachexia by the secretion of pro-inflammatory cytokines, such as Tumor Necrosis Factor-? (TNF-?), Interferon- ? (IFN-?) and Interleukin-6. The establishment of chronic inflammation increases the mobilization of glucose precursors and proteolysis in muscle tissue, negatively impacting energy balance and inducing loss of body weight. Furthermore, cachexia-induced activation of glycolysis and mitochondrial dysfunction increase lactic acid in muscles, reducing energy production via the Krebs cycle. Thus, the metabolic dysfunction induced by cachexia involves several pathways, complicating development of valid treatments. A full understanding of all players that cause alterations in muscle metabolism is necessary to identify new specific targets and develop new combined pharmacological approaches to counteract or, at least, delay muscle wasting.
We welcome submissions of Original Research, Review, Mini-reviews, Opinions, Methods, and Perspective articles that cover, but are not limited to, the following topics:
• Novel targets involved in the transcriptional, post-transcriptional, and post-translational regulation of muscle metabolism
• New strategies to modulate the secretion of pro-inflammatory cytokines in patients affected by cachexia
• Use of small molecules to counteract muscle wasting
• Effects of nutrients, hormones, and physical exercise in the controlling muscle metabolism
• Roles of gender difference in metabolic response to drug treatment
• Efficacy of combined pharmacological and cognitive-behavioral therapies to delay muscle atrophy
• Modulation of mitochondrial dysfunction to rescue the loss of energy production
• The impact of oxidative stress on the onset of cachexia
Skeletal muscle is a specialized contractile tissue with crucial roles in the regulation of systemic energy homeostasis. In particular, skeletal muscle is the most important site for glucose metabolism and for fatty acid oxidation. Along this line, it is considered a reservoir of amino acids that can be released as needed, supporting protein synthesis and energy production in the organism. Interestingly, skeletal muscle can adapt its metabolic role in response to physiological and pathological conditions. Several diseases, such as cancer/immune disorders/muscular dystrophies, are characterized by an increased level of cytokines, which induce chronic inflammation in the organism. This condition causes a reduction in protein synthesis and an enhancement in catabolism in muscle tissue, affecting energy balance and leading to the onset of cachexia.
During the last decades, several studies demonstrated that inflammation plays a crucial role in controlling metabolism in patients affected by cachexia by the secretion of pro-inflammatory cytokines, such as Tumor Necrosis Factor-? (TNF-?), Interferon- ? (IFN-?) and Interleukin-6. The establishment of chronic inflammation increases the mobilization of glucose precursors and proteolysis in muscle tissue, negatively impacting energy balance and inducing loss of body weight. Furthermore, cachexia-induced activation of glycolysis and mitochondrial dysfunction increase lactic acid in muscles, reducing energy production via the Krebs cycle. Thus, the metabolic dysfunction induced by cachexia involves several pathways, complicating development of valid treatments. A full understanding of all players that cause alterations in muscle metabolism is necessary to identify new specific targets and develop new combined pharmacological approaches to counteract or, at least, delay muscle wasting.
We welcome submissions of Original Research, Review, Mini-reviews, Opinions, Methods, and Perspective articles that cover, but are not limited to, the following topics:
• Novel targets involved in the transcriptional, post-transcriptional, and post-translational regulation of muscle metabolism
• New strategies to modulate the secretion of pro-inflammatory cytokines in patients affected by cachexia
• Use of small molecules to counteract muscle wasting
• Effects of nutrients, hormones, and physical exercise in the controlling muscle metabolism
• Roles of gender difference in metabolic response to drug treatment
• Efficacy of combined pharmacological and cognitive-behavioral therapies to delay muscle atrophy
• Modulation of mitochondrial dysfunction to rescue the loss of energy production
• The impact of oxidative stress on the onset of cachexia
