IL-6-induced skeletal muscle atrophy.

By F. Haddad, F. Zaldivar, D. Cooper, G. Adams. Journal of applied physiology, 2005

639 citations recorded by the source corpus.

Chronic, low-level elevation of circulating interleukin (IL)-6 is observed in disease states as well as in many outwardly healthy elderly individuals. Increased plasma IL-6 is also observed after intense, prolonged exercise. In the context of skeletal muscle, IL-6 has variously been reported to regulate carbohydrate and lipid metabolism, increase satellite cell proliferation, or cause muscle wasting. In the present study, we used a rodent local infusion model to deliver modest levels of IL-6, comparable to that present after exercise or with chronic low-level inflammation in the elderly, directly into a single target muscle in vivo. The aim of this study was to examine the direct effects of IL-6 on skeletal muscle in the absence of systemic changes in this cytokine. Data included cellular and molecular markers of cytokine and growth factor signaling (phosphorylation and mRNA content) as well as measurements to detect muscle atrophy. IL-6 infusion resulted in muscle atrophy characterized by a preferential loss of myofibrillar protein (-17%). IL-6 induced a decrease in the phosphorylation of ribosomal S6 kinase (-60%) and STAT5 (-33%), whereas that of STAT3 was increased approximately twofold. The changes seen in the IL-6-infused muscles suggest alterations in the balance of growth factor-related signaling in favor of a more catabolic profile. This suggests that downregulation of growth factor-mediated intracellular signaling may be a mechanism contributing to the development of muscle atrophy induced by elevated IL-6.

Subfields: Molecular Biology, Psychiatry and Mental health, Rehabilitation

View Paper: https://www.semanticscholar.org/paper/d763bad07016f11f567ebe250d4ce3c07046238a

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Citations in the corpus

Interleukin-6 is an essential regulator of satellite cell-mediated skeletal muscle hypertrophy. (2008, background): “Notably, the beneﬁcial function of local and transiently produced IL-6isopposedtotheknownmuscle-wastingeffectofinfusedIL-6 or systemic high levels of IL-6 in cachectic conditions (Haddad et al., 2005; Tisdale, 2005).”
Interleukin-6 in aging and chronic disease: a magnificent pathway. (2006, background): “increased STAT phosphorylation in favor of a more catabolic profile (101).”
The role of exercise and PGC1α in inflammation and chronic disease (2008, background): “Finally, a chronic increase in IL-6 and TNF-α concentrations results in atrophy of skeletal muscle and inhibition of muscle regeneration, respectivel”