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Review
. 2024 Dec;602(23):6587-6607.
doi: 10.1113/JP284808. Epub 2023 Aug 10.

Inflammation o'clock: interactions of circadian rhythms with inflammation-induced skeletal muscle atrophy

Affiliations
Review

Inflammation o'clock: interactions of circadian rhythms with inflammation-induced skeletal muscle atrophy

Francielly Morena da Silva et al. J Physiol. 2024 Dec.

Abstract

Circadian rhythms are ∼24 h cycles evident in behaviour, physiology and metabolism. The molecular mechanism directing circadian rhythms is the circadian clock, which is composed of an interactive network of transcription-translation feedback loops. The core clock genes include Bmal1, Clock, Rev-erbα/β, Per and Cry. In addition to keeping time, the core clock regulates a daily programme of gene expression that is important for overall cell homeostasis. The circadian clock mechanism is present in all cells, including skeletal muscle fibres, and disruption of the muscle clock is associated with changes in muscle phenotype and function. Skeletal muscle atrophy is largely associated with a lower quality of life, frailty and reduced lifespan. Physiological and genetic modification of the core clock mechanism yields immune dysfunction, alters inflammatory factor expression and secretion and is associated with skeletal muscle atrophy in multiple conditions, such as ageing and cancer cachexia. Here, we summarize the possible interplay between the circadian clock modulation of immune cells, systemic inflammatory status and skeletal muscle atrophy in chronic inflammatory conditions. Although there is a clear disruption of circadian clocks in various models of atrophy, the mechanism behind such alterations remains unknown. Understanding the modulatory potential of muscle and immune circadian clocks in inflammation and skeletal muscle health is essential for the development of therapeutic strategies to protect skeletal muscle mass and function of patients with chronic inflammation.

Keywords: ageing; cancer cachexia; immune system; muscle clock; skeletal muscle; type 2 diabetes mellitus.

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Conflict of interest statement

Competing interests

The authors declare no conflict of interest.

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References

    1. Afzali AM, Müntefering T, Wiendl H, Meuth SG, & Ruck T (2018). Skeletal muscle cells actively shape (auto)immune responses. Autoimmunity Reviews, 17(5), 518–529. - PubMed
    1. Aguilar-Arnal L, Hakim O, Patel VR, Baldi P, Hager GL, & Sassone-Corsi P (2013). Cycles in spatial and temporal chromosomal organization driven by the circadian clock. Nature Structural & Molecular Biology, 20(10), 1206–1213. - PMC - PubMed
    1. Amir M, Campbell S, Kamenecka TM, & Solt LA (2020). Pharmacological modulation and genetic deletion of REV-ERBα and REV-ERBβ regulates dendritic cell development. Biochemical and Biophysical Research Communications, 527(4), 1000–1007. - PMC - PubMed
    1. Anderson LJ, Liu H, & Garcia JM (2017). Sex Differences in Muscle Wasting. Advances in Experimental Medicine and Biology, 1043, 153–197. - PubMed
    1. Andrews JL, Zhang X, McCarthy JJ, McDearmon EL, Hornberger TA, Russell B, Campbell KS, Arbogast S, Reid MB, Walker JR, Hogenesch JB, Takahashi JS, & Esser KA (2010). CLOCK and BMAL1 regulate MyoD and are necessary for maintenance of skeletal muscle phenotype and function. Proceedings of the National Academy of Sciences, 107(44), 19090–19095. - PMC - PubMed

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