Purpose of review 

This review will update clinicians and basic scientists who study the molecular mechanisms of muscle wasting associated with infection, trauma, cancer cachexia, and AIDS. A special emphasis is placed on recent studies that examine the interaction of insulin-like growth factor 1 and proinflammatory cytokines as positive and negative regulators of muscle mass.

Recent findings 

Potential mediators of the wasting syndromes include catabolic hormones, such as glucocorticoids, as well as the inflammatory cytokines tumour necrosis factor, IL-1, and IL-6. Cytokines may function either systemically or locally within muscle per se. Lipopolysaccharide and other pathogen-associated molecules stimulate cytokine expression in muscle. The failure to clear pathogen-associated molecules or the introduction of muscle damage may initiate a protracted activation of enzymes and transcription factors that orchestrate a genetic programme that ultimately produces muscle wasting.

Summary 

This review highlights recent advances in our understanding of the expression of the afferent and efferent limbs of the innate immune system in skeletal muscle. A special emphasis is placed on the recognition of pathogen-associated molecules by skeletal muscle cells and how these molecules regulate the expression of inflammatory cytokines and other muscle genes to result in muscle wasting, and when sustained, the erosion of lean body mass.