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. 2022:1363:35-70.
doi: 10.1007/978-3-030-92034-0_4.

Long Non-coding RNAs in Rheumatology

Affiliations

Long Non-coding RNAs in Rheumatology

Susanne N Wijesinghe et al. Adv Exp Med Biol. 2022.

Abstract

The last decade has seen an enormous increase in long non-coding RNA (lncRNA) research within rheumatology. LncRNAs are arbitrarily classed as non-protein encoding RNA transcripts that exceed 200 nucleotides in length. These transcripts have tissue and cell specific patterns of expression and are implicated in a variety of biological processes. Unsurprisingly, numerous lncRNAs are dysregulated in rheumatoid conditions, correlating with disease activity and cited as potential biomarkers and targets for therapeutic intervention. In this chapter, following an introduction into each condition, we discuss the lncRNAs involved in rheumatoid arthritis, osteoarthritis and systemic lupus erythematosus. These inflammatory joint conditions share several inflammatory signalling pathways and therefore not surprisingly many commonly dysregulated lncRNAs are shared across these conditions. In the interest of translational research only those lncRNAs which are strongly conserved have been addressed. The lncRNAs discussed here have diverse roles in regulating inflammation, proliferation, migration, invasion and apoptosis. Understanding the molecular basis of lncRNA function in rheumatology will be crucial in fully determining the inflammatory mechanisms that drive these conditions.

Keywords: Inflammation; Long noncoding RNA; Osteoarthritis; Rheumatoid arthritis; Systemic lupus erythematosus.

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References

    1. Guo Q, Wang Y, Xu D, Nossent J, Pavlos NJ, Xu J (2018) Rheumatoid arthritis: pathological mechanisms and modern pharmacologic therapies. Bone Res 6:15. https://doi.org/10.1038/s41413-018-0016-9 - DOI
    1. Crowson CS, Matteson EL, Myasoedova E et al (2011) The lifetime risk of adult-onset rheumatoid arthritis and other inflammatory autoimmune rheumatic diseases. Arthritis Rheum 63(3):633–639. https://doi.org/10.1002/art.30155 - DOI
    1. Xu B, Lin J (2017) Characteristics and risk factors of rheumatoid arthritis in the United States: an NHANES analysis. Peer J 5:e4035. https://doi.org/10.7717/peerj.4035 - DOI
    1. Fukui S, Iwamoto N, Takatani A et al (2017) M1 and M2 monocytes in rheumatoid arthritis: a contribution of imbalance of M1/M2 monocytes to Osteoclastogenesis. Front Immunol 8:1958. https://doi.org/10.3389/fimmu.2017.01958 - DOI
    1. Kung CC, Dai SP, Chiang H, Huang HS, Sun WH (2020) Temporal expression patterns of distinct cytokines and M1/M2 macrophage polarization regulate rheumatoid arthritis progression. Mol Biol Rep 47(5):3423–3437. https://doi.org/10.1007/s11033-020-05422-6 - DOI

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