학술논문
Adiponectin Deregulation in Systemic Autoimmune Rheumatic Diseases.
Document Type
Academic Journal
Author
Brezovec N; Department of Rheumatology, University Medical Centre Ljubljana, 1000 Ljubljana, Slovenia.; Faculty of Pharmacy, University of Ljubljana, 1000 Ljubljana, Slovenia.; Perdan-Pirkmajer K; Department of Rheumatology, University Medical Centre Ljubljana, 1000 Ljubljana, Slovenia.; Faculty of Medicine, University of Ljubljana, 1000 Ljubljana, Slovenia.; Čučnik S; Department of Rheumatology, University Medical Centre Ljubljana, 1000 Ljubljana, Slovenia.; Faculty of Pharmacy, University of Ljubljana, 1000 Ljubljana, Slovenia.; Sodin-Šemrl S; Department of Rheumatology, University Medical Centre Ljubljana, 1000 Ljubljana, Slovenia.; FAMNIT, University of Primorska, 6000 Koper, Slovenia.; Varga J; Department of Internal Medicine, University of Michigan, Ann Arbor, MI 48109, USA.; Lakota K; Department of Rheumatology, University Medical Centre Ljubljana, 1000 Ljubljana, Slovenia.; FAMNIT, University of Primorska, 6000 Koper, Slovenia.
Source
Publisher: MDPI Country of Publication: Switzerland NLM ID: 101092791 Publication Model: Electronic Cited Medium: Internet ISSN: 1422-0067 (Electronic) Linking ISSN: 14220067 NLM ISO Abbreviation: Int J Mol Sci Subsets: MEDLINE
Subject
Language
English
Abstract
Deregulation of adiponectin is found in systemic autoimmune rheumatic diseases (SARDs). Its expression is downregulated by various inflammatory mediators, but paradoxically, elevated serum levels are present in SARDs with high inflammatory components, such as rheumatoid arthritis and systemic lupus erythematosus. Circulating adiponectin is positively associated with radiographic progression in rheumatoid arthritis as well as with cardiovascular risks and lupus nephritis in systemic lupus erythematosus. However, in SARDs with less prominent inflammation, such as systemic sclerosis, adiponectin levels are low and correlate negatively with disease activity. Regulators of adiponectin gene expression (PPAR-γ, Id3, ATF3, and SIRT1) and inflammatory cytokines (interleukin 6 and tumor necrosis factor α) are differentially expressed in SARDs and could therefore influence total adiponectin levels. In addition, anti-inflammatory therapy could also have an impact, as tocilizumab treatment is associated with increased serum adiponectin. However, anti-tumor necrosis factor α treatment does not seem to affect its levels. Our review provides an overview of studies on adiponectin levels in the bloodstream and other biological samples from SARD patients and presents some possible explanations why adiponectin is deregulated in the context of therapy and gene regulation.