期刊
EXPERIMENTAL PHYSIOLOGY
卷 98, 期 1, 页码 19-24出版社
WILEY-BLACKWELL
DOI: 10.1113/expphysiol.2011.063321
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类别
资金
- NIH [AR041705, AR060217]
- NATIONAL INSTITUTE OF ARTHRITIS AND MUSCULOSKELETAL AND SKIN DISEASES [R01AR041705, R29AR041705, R01AR060217] Funding Source: NIH RePORTER
The nuclear factor-kappa B (NF-kappa B) signalling pathway is a necessary component of adult skeletal muscle atrophy resulting from systemic illnesses or disuse. Studies showing a role for the NF-kappa B pathway in muscle disuse include unloading, denervation and immobilization, and studies showing a role for NF-kappa B 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-kappa B transcriptional activity. With the exception of muscle unloading, however, there is a paucity of data on the NF-kappa B transcription factors that regulate muscle atrophy, and little is known about which genes are targeted by NF-kappa B transcription factors during atrophy. Interestingly, in some cases it appears that the amelioration of muscle atrophy by genetic inhibition of NF-kappa B signalling proteins is due to effects that are independent of the downstream NF-kappa B transcription factors. These questions are prime areas for investigation if we are to understand a key component of muscle wasting in adult skeletal muscle.
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