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Review
. 2016:2016:1438686.
doi: 10.1155/2016/1438686. Epub 2016 Jun 13.

MicroRNA-Regulated Proinflammatory Cytokines in Sarcopenia

Jingjing Fan  1 , Xianjuan Kou  1 , Yi Yang  1 , Ning Chen  1
Affiliations
Review

MicroRNA-Regulated Proinflammatory Cytokines in Sarcopenia

Jingjing Fan et al. Mediators Inflamm. 2016.

Abstract

Sarcopenia has been defined as the aging-related disease with the declined mass, strength, and function of skeletal muscle, which is the major cause of frailty and falls in elders. The activation of inflammatory signal pathways due to diseases and aging is suggested to reveal the critical impact on sarcopenia. Several proinflammatory cytokines, especially interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-α), play crucial roles in modulation of inflammatory signaling pathway during the aging-related loss of skeletal muscle. MicroRNAs (miRNAs) have emerged as the important regulators for the mass and functional maintenance of skeletal muscle through regulating gene expression of proinflammatory cytokines. In this paper, we have systematically discussed regulatory mechanisms of miRNAs for the expression and secretion of inflammatory cytokines during sarcopenia, which will provide some novel targets and therapeutic strategies for controlling aging-related atrophy of skeletal muscle and corresponding chronic inflammatory diseases.

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Figures

Figure 1
Figure 1
The interplay between sarcopenia and chronic inflammation. The boxes represent domains known to influence the maintenance of sarcopenia and inflammation response in aging organisms. Abbreviations: ROS, reactive oxygen species.
See this image and copyright information in PMC

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References

    1. Morley J. E., Anker S. D., von Haehling S. Prevalence, incidence, and clinical impact of sarcopenia: facts, numbers, and epidemiology—update 2014. Journal of Cachexia, Sarcopenia and Muscle. 2014;5(4):253–259. doi: 10.1007/s13539-014-0161-y. - DOI - PMC - PubMed
    1. Fan J., Kou X., Jia S., Yang X., Yang Y., Chen N. Autophagy as a potential target for sarcopenia. Journal of Cellular Physiology. 2016;231(7):1450–1459. doi: 10.1002/jcp.25260. - DOI - PubMed
    1. Kandarian S. C., Jackman R. W. Intracellular signaling during skeletal muscle atrophy. Muscle and Nerve. 2006;33(2):155–165. doi: 10.1002/mus.20442. - DOI - PubMed
    1. White J. R., Confides A. L., Moore-Reed S., Hoch J. M., Dupont-Versteegden E. E. Regrowth after skeletal muscle atrophy is impaired in aged rats, despite similar responses in signaling pathways. Experimental Gerontology. 2015;64:17–32. doi: 10.1016/j.exger.2015.02.007. - DOI - PMC - PubMed
    1. Kaasik P., Umnova M., Pehme A., et al. Ageing and dexamethasone associated sarcopenia: peculiarities of regeneration. Journal of Steroid Biochemistry and Molecular Biology. 2007;105(1–5):85–90. doi: 10.1016/j.jsbmb.2006.11.024. - DOI - PubMed