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核因子-κB 信号转导与骨骼肌萎缩的转录调控

Nuclear factor-κB signalling and transcriptional regulation in skeletal muscle atrophy.

机构信息

Boston University, Department of Health Sciences, 635 Commonwealth Avenue, Boston, MA 02215, USA.

出版信息

Exp Physiol. 2013 Jan;98(1):19-24. doi: 10.1113/expphysiol.2011.063321. Epub 2012 Jul 30.

DOI:10.1113/expphysiol.2011.063321
PMID:22848079
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3505235/
Abstract

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.

摘要

核因子-κB(NF-κB)信号通路是全身性疾病或废用导致成人骨骼肌萎缩的必要组成部分。研究表明,NF-κB 通路在肌肉废用中的作用包括去负荷、去神经和固定,而 NF-κB 在全身性疾病中的作用包括癌症、慢性心力衰竭和急性脓毒症肺损伤。大多数这些触发因素引起的肌肉萎缩与 NF-κB 转录活性的激活有关。然而,除肌肉去负荷外,关于调节肌肉萎缩的 NF-κB 转录因子的数据很少,并且对于 NF-κB 转录因子在萎缩过程中靶向哪些基因知之甚少。有趣的是,在某些情况下,通过遗传抑制 NF-κB 信号蛋白来改善肌肉萎缩似乎是由于与下游 NF-κB 转录因子无关的作用。如果我们要了解成年骨骼肌中肌肉消耗的关键组成部分,这些问题是主要的研究领域。

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本文引用的文献

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