Nuclear factor‐κB signalling and transcriptional regulation in skeletal muscle atrophy

• Published in: Experimental physiology Vol. 98; no. 1; pp. 19 - 24
• Main Authors: Jackman, Robert W., Cornwell, Evangeline W., Wu, Chia‐Ling, Kandarian, Susan C.
• Format: Journal Article
• Language: English
• Published: Oxford, UK Blackwell Publishing Ltd 01.01.2013
• Subjects: Adult; Animals; Gene Expression Regulation; Humans; Mice; Muscle, Skeletal - pathology; Muscular Atrophy - metabolism; Muscular Atrophy - pathology; NF-kappa B - physiology; Signal Transduction - drug effects; Signal Transduction - physiology; Transcription Factors - physiology; Transcriptional Activation - physiology
• DOI: 10.1113/expphysiol.2011.063321
• ISSN: 0958-0670; 1469-445X

New findings •  What is the topic for this review? An up‐to‐date analysis on the role of nuclear factor‐κB signaling and transcriptional control in adult skeletal muscle atrophy. •  What advances does it highlight? Our analysis of the literature and research in our laboratory has allowed us to propose interpretations that have not previously been published. We believe these interpretations will be of interest to scientists studying the cellular control of adult skeletal muscle atrophy. The nuclear factor‐κB (NF‐κB) signalling pathway is a necessary component of adult skeletal muscle atrophy resulting from systemic illnesses or disuse. Studies showing a role for the NF‐κB pathway in muscle disuse include unloading, denervation and immobilization, and studies showing a role for NF‐κB in systemic illnesses include cancer, chronic heart failure and acute septic lung injury. Muscle atrophy due to most of these triggers is associated with activation of NF‐κB transcriptional activity. With the exception of muscle unloading, however, there is a paucity of data on the NF‐κB transcription factors that regulate muscle atrophy, and little is known about which genes are targeted by NF‐κB transcription factors during atrophy. Interestingly, in some cases it appears that the amelioration of muscle atrophy by genetic inhibition of NF‐κB signalling proteins is due to effects that are independent of the downstream NF‐κB transcription factors. These questions are prime areas for investigation if we are to understand a key component of muscle wasting in adult skeletal muscle.