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      Sarcopenia in Autoimmune and Rheumatic Diseases: A Comprehensive Review

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          Abstract

          Sarcopenia refers to a decrease in skeletal muscle mass and function. Because sarcopenia affects mortality, and causes significant disability, the clinical importance of sarcopenia is emerging. At first, sarcopenia was recognized as an age-related disease but, recently, it has been reported to be prevalent also in younger patients with autoimmune diseases. Specifically, the association of sarcopenia and autoimmune diseases such as rheumatoid arthritis has been studied in detail. Although the pathogenesis of sarcopenia in autoimmune diseases has not been elucidated, chronic inflammation is believed to contribute to sarcopenia, and moreover the pathogenesis seems to be different depending on the respective underlying disease. The definition of sarcopenia differs among studies, which limits direct comparisons. Therefore, in this review, we cover various definitions of sarcopenia used in previous studies and highlight the prevalence of sarcopenia in diverse autoimmune diseases including rheumatoid arthritis, spondyloarthritis, systemic sclerosis, inflammatory bowel disease, and autoimmune diabetes. In addition, we cover the pathogenesis and treatment of sarcopenia in autoimmune and rheumatic diseases. This review provides a comprehensive understanding of sarcopenia in various autoimmune diseases and highlights the need for a consistent definition of sarcopenia.

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          The microbiome in inflammatory bowel disease: current status and the future ahead.

          Studies of the roles of microbial communities in the development of inflammatory bowel disease (IBD) have reached an important milestone. A decade of genome-wide association studies and other genetic analyses have linked IBD with loci that implicate an aberrant immune response to the intestinal microbiota. More recently, profiling studies of the intestinal microbiome have associated the pathogenesis of IBD with characteristic shifts in the composition of the intestinal microbiota, reinforcing the view that IBD results from altered interactions between intestinal microbes and the mucosal immune system. Enhanced technologies can increase our understanding of the interactions between the host and its resident microbiota and their respective roles in IBD from both a large-scale pathway view and at the metabolic level. We review important microbiome studies of patients with IBD and describe what we have learned about the mechanisms of intestinal microbiota dysfunction. We describe the recent progress in microbiome research from exploratory 16S-based studies, reporting associations of specific organisms with a disease, to more recent studies that have taken a more nuanced view, addressing the function of the microbiota by metagenomic and metabolomic methods. Finally, we propose study designs and methodologies for future investigations of the microbiome in patients with inflammatory gut and autoimmune diseases in general. Copyright © 2014 AGA Institute. Published by Elsevier Inc. All rights reserved.
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            Welcome to the ICD‐10 code for sarcopenia

            Abstract The new ICD‐10‐CM (M62.84) code for sarcopenia represents a major step forward in recognizing sarcopenia as a disease. This should lead to an increase in availability of diagnostic tools and the enthusiasm for pharmacological companies to develop drugs for sarcopenia.
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              Interleukin‐6 myokine signaling in skeletal muscle: a double‐edged sword?

              Interleukin (IL)‐6 is a cytokine with pleiotropic functions in different tissues and organs. Skeletal muscle produces and releases significant levels of IL‐6 after prolonged exercise and is therefore considered as a myokine. Muscle is also an important target of the cytokine. IL‐6 signaling has been associated with stimulation of hypertrophic muscle growth and myogenesis through regulation of the proliferative capacity of muscle stem cells. Additional beneficial effects of IL‐6 include regulation of energy metabolism, which is related to the capacity of actively contracting muscle to synthesize and release IL‐6. Paradoxically, deleterious actions for IL‐6 have also been proposed, such as promotion of atrophy and muscle wasting. We review the current evidence for these apparently contradictory effects, the mechanisms involved and discuss their possible biological implications.
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                Author and article information

                Journal
                Int J Mol Sci
                Int J Mol Sci
                ijms
                International Journal of Molecular Sciences
                MDPI
                1422-0067
                07 August 2020
                August 2020
                : 21
                : 16
                : 5678
                Affiliations
                [1 ]Yonsei University College of Medicine, Seoul 03722, Korea; hjj622@ 123456yonsei.ac.kr
                [2 ]Laboratory Microorganismes and Active Biomolecules, Sciences Faculty of Tunis, University Tunis El Manar, Tunis 2092, Tunisia; kalttizaoui@ 123456gmail.com
                [3 ]Department of Pharmaceutical Sciences and Interdepartmental Research Center of Pharmacogenetics and Pharmacogenomics (CRIFF), University of Piemonte Orientale, 28100 Novara, Italy; salvatore.terrazzino@ 123456uniupo.it (S.T.); sarah.cargnin@ 123456uniupo.it (S.C.)
                [4 ]Department of Pediatrics, Yonsei University College of Medicine, Seoul 03722, Korea; AZSAGM@ 123456yuhs.ac
                [5 ]Department of Rheumatology, Wonju Severance Christian Hospital, Yonsei University Wonju College of Medicine, Wonju 26426, Korea; namsw@ 123456yonsei.ac.kr
                [6 ]Department of Nephrology, Yonsei University Wonju College of Medicine, Wonju 26426, Korea; ripplesong@ 123456yonsei.ac.kr (J.S.K.); kidney74@ 123456yonsei.ac.kr (J.W.Y.); junyoung07@ 123456yonsei.ac.kr (J.Y.L.)
                [7 ]The Cambridge Centre for Sport and Exercise Science, Anglia Ruskin University, Cambridge CB1 1PT, UK; Lee.Smith@ 123456anglia.ac.uk
                [8 ]Research and Development Unit, Parc Sanitari Sant Joan de Déu, CIBERSAM, 08830 Barcelona, Spain; a.koyanagi@ 123456pssjd.org (A.K.); louis.jacob.contacts@ 123456gmail.com (L.J.)
                [9 ]ICREA, Pg. Lluis Companys 23, 08010 Barcelona, Spain
                [10 ]Faculty of Medicine, University of Versailles Saint-Quentin-en-Yvelines, 78000 Versailles, France
                [11 ]University of Florida College of Medicine, Gainesville, FL 32610, USA; lih2@ 123456ufl.edu
                [12 ]Department of Internal Medicine IV (Nephrology and Hypertension), Medical University Innsbruck, 6020 Innsbruck, Austria; Andreas.Kronbichler@ 123456i-med.ac.at
                Author notes
                [* ]Correspondence: SHINJI@ 123456yuhs.ac ; Tel.: +82-2-22282-050
                Author information
                https://orcid.org/0000-0002-4909-1121
                https://orcid.org/0000-0001-6242-7817
                https://orcid.org/0000-0002-1511-9587
                https://orcid.org/0000-0003-3689-5865
                https://orcid.org/0000-0001-8047-4190
                https://orcid.org/0000-0002-5340-9833
                https://orcid.org/0000-0002-9565-5004
                https://orcid.org/0000-0003-1071-1239
                https://orcid.org/0000-0002-9800-9948
                https://orcid.org/0000-0003-2326-1820
                https://orcid.org/0000-0002-2945-2946
                Article
                ijms-21-05678
                10.3390/ijms21165678
                7461030
                32784808
                dd1c1be9-e8d7-4ebf-bd09-dfcce702a6a7
                © 2020 by the authors.

                Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license ( http://creativecommons.org/licenses/by/4.0/).

                History
                : 09 July 2020
                : 03 August 2020
                Categories
                Review

                Molecular biology
                sarcopenia,rheumatic disease,autoimmune disease,rheumatoid arthritis,inflammatory bowel disease,type 1 diabetes

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