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Archives of Physiology and Biochemistry
The Journal of Metabolic Diseases
Volume 128, 2022 - Issue 6
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Review Article

The interrelationship between inflammatory cytokines and skeletal muscle decay from the viewpoint of circadian rhythms

, , , , &
Pages 1559-1565 | Received 23 Oct 2019, Accepted 09 Jun 2020, Published online: 01 Jul 2020
 

Abstract

Circadian rhythms affect a variety of physiological processes. Disruption of circadian rhythms causes many diseases, most of which are associated with inflammation. Disruption of circadian rhythms has a detrimental impact on the function of immune system. It is common to find that circulatory LPS are increased. LPS induces immune cells to produce inflammatory cytokines. Inflammatory cytokines play a role in skeletal muscle decay. Rev-erbβ has been identified as a critical regulator of circadian rhythms and a factor in inflammation. Another effect of disruption is a concomitant disturbance of glucose–insulin metabolism, which skeletal muscle likely contributes to considering it is a key metabolic tissue. Disruption of circadian rhythms is also related to obesity. Obesity can cause an increase expression of inflammatory cytokines. Maybe obesity with skeletal muscle decay is one of major characteristics. Future studies are needed to obtain a comprehensive understanding of inflammatory cytokines and skeletal muscle decay from the viewpoint of circadian rhythms.

Disclosure statement

The authors report no conflicts of interest. The authors alone are responsible for the content and writing of the paper.

Author contributions

Xuguang Luo and Xinhua Yang contributed equally to this work. All authors provided acquisition of data and gave final approval of the manuscript submitted.

Additional information

Funding

The project was partially supported by Natural Science Foundation of Shanxi Province, China [Grant no. 201901D111185], Natural Science Foundation of Shanxi Province, China [Grant no. 2014021028–1], Science and Technology Innovation Fund of Shanxi Medical University [Grant no. 01201401] to XMC.

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