Adipokine role in physiopathology of inflammatory and degenerative musculoskeletal diseases

被引:16
|
作者
Giardullo, Liberato [1 ]
Corrado, Addolorata [1 ]
Maruotti, Nicola [1 ]
Cici, Daniela [1 ]
Mansueto, Natalia [1 ]
Cantatore, Francesco Paolo [1 ]
机构
[1] Univ Foggia, Policlin Riuniti Univ Hosp, Dept Med & Surg Sci, Rheumatol Clin Mario Carrozzo, Viale Pinto 1, I-71122 Foggia, Italy
关键词
adipokines; adiponectin; autoimmune; rheumatology; leptin; JUVENILE IDIOPATHIC ARTHRITIS; SYSTEMIC-LUPUS-ERYTHEMATOSUS; NECROSIS-FACTOR-ALPHA; BINDING-PROTEIN; 4; ADIPOSE-TISSUE; TNF-ALPHA; SERUM-LEVELS; RHEUMATOID-ARTHRITIS; INSULIN-RESISTANCE; GENE-EXPRESSION;
D O I
10.1177/20587384211015034
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
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.
引用
收藏
页数:17
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