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      Adipokine role in physiopathology of inflammatory and degenerative musculoskeletal diseases

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          Abstract

          We performed a systematic literature review to summarize the underlying pathogenic mechanisms by which adipokines influence rheumatological diseases and the resulting clinical manifestations. Increasing evidence display that numerous adipokines may significantly influence the development or clinical course of various rheumatological diseases. Despite the normal anti- or pro-inflammatory role of the cytokines, the serum level varies enormously in various rheumatological diseases. The expression of high levels of pro-inflammatory cytokines such as leptin or visfatin, respectively in systemic lupus erythematosus and in rheumatoid arthritis, represents a negative prognostic factor; other adipokines such as adiponectin, broadly known for their anti-inflammatory effects, showed a correlation with disease activity in rheumatoid arthritis. In the near future pro-inflammatory cytokines may represent a potential therapeutic target to restrain the severity of rheumatological diseases. Further studies on adipokines may provide important information on the pathogenesis of these diseases, which are not yet fully understood. The mechanisms by which adipokines induce, worsen, or suppress inflammatory and degenerative musculoskeletal pathologies and their clinical significance will be discussed in this review.

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          Positional cloning of the mouse obese gene and its human homologue.

          The mechanisms that balance food intake and energy expenditure determine who will be obese and who will be lean. One of the molecules that regulates energy balance in the mouse is the obese (ob) gene. Mutation of ob results in profound obesity and type II diabetes as part of a syndrome that resembles morbid obesity in humans. The ob gene product may function as part of a signalling pathway from adipose tissue that acts to regulate the size of the body fat depot.
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            Adipose tissue as an endocrine organ.

            Adipose tissue is a complex, essential, and highly active metabolic and endocrine organ. Besides adipocytes, adipose tissue contains connective tissue matrix, nerve tissue, stromovascular cells, and immune cells. Together these components function as an integrated unit. Adipose tissue not only responds to afferent signals from traditional hormone systems and the central nervous system but also expresses and secretes factors with important endocrine functions. These factors include leptin, other cytokines, adiponectin, complement components, plasminogen activator inhibitor-1, proteins of the renin-angiotensin system, and resistin. Adipose tissue is also a major site for metabolism of sex steroids and glucocorticoids. The important endocrine function of adipose tissue is emphasized by the adverse metabolic consequences of both adipose tissue excess and deficiency. A better understanding of the endocrine function of adipose tissue will likely lead to more rational therapy for these increasingly prevalent disorders. This review presents an overview of the endocrine functions of adipose tissue.
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              Low-grade inflammation as a key mediator of the pathogenesis of osteoarthritis.

              Osteoarthritis (OA) has long been viewed as a degenerative disease of cartilage, but accumulating evidence indicates that inflammation has a critical role in its pathogenesis. Furthermore, we now appreciate that OA pathogenesis involves not only breakdown of cartilage, but also remodelling of the underlying bone, formation of ectopic bone, hypertrophy of the joint capsule, and inflammation of the synovial lining. That is, OA is a disorder of the joint as a whole, with inflammation driving many pathologic changes. The inflammation in OA is distinct from that in rheumatoid arthritis and other autoimmune diseases: it is chronic, comparatively low-grade, and mediated primarily by the innate immune system. Current treatments for OA only control the symptoms, and none has been FDA-approved for the prevention or slowing of disease progression. However, increasing insight into the inflammatory underpinnings of OA holds promise for the development of new, disease-modifying therapies. Indeed, several anti-inflammatory therapies have shown promise in animal models of OA. Further work is needed to identify effective inhibitors of the low-grade inflammation in OA, and to determine whether therapies that target this inflammation can prevent or slow the development and progression of the disease.
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                Author and article information

                Journal
                Int J Immunopathol Pharmacol
                Int J Immunopathol Pharmacol
                IJI
                spiji
                International Journal of Immunopathology and Pharmacology
                SAGE Publications (Sage UK: London, England )
                0394-6320
                2058-7384
                13 May 2021
                Jan-Dec 2021
                : 35
                : 20587384211015034
                Affiliations
                [1-20587384211015034]Rheumatology Clinic “Mario Carrozzo”, Department of Medical and Surgical Sciences, University of Foggia, “Policlinico Riuniti” University Hospital, Foggia, Italy
                Author notes
                [*]Liberato Giardullo, Rheumatology Clinic “Mario Carrozzo”, Department of Medical and Surgical Sciences, University of Foggia, “Policlinico Riuniti” University Hospital, Viale Pinto, 1, Foggia 71122, Italy. Email: liberato.giardullo@ 123456gmail.com
                Author information
                https://orcid.org/0000-0003-1655-0608
                Article
                10.1177_20587384211015034
                10.1177/20587384211015034
                8127732
                33983056
                53dc399b-7ddc-4557-8b27-e8f14beb7900
                © The Author(s) 2021

                This article is distributed under the terms of the Creative Commons Attribution-NonCommercial 4.0 License ( https://creativecommons.org/licenses/by-nc/4.0/) which permits non-commercial use, reproduction and distribution of the work without further permission provided the original work is attributed as specified on the SAGE and Open Access pages ( https://us.sagepub.com/en-us/nam/open-access-at-sage).

                History
                : 8 December 2020
                : 5 April 2021
                Categories
                Original Research Article
                Custom metadata
                January-December 2021
                ts1

                adipokines,adiponectin,autoimmune,rheumatology,leptin
                adipokines, adiponectin, autoimmune, rheumatology, leptin

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