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风湿性关节疾病中的脂肪因子网络。

The Adipokine Network in Rheumatic Joint Diseases.

机构信息

Department of Cellular Biology, Faculty of Biology, Complutense University, 28040 Madrid, Spain.

Department of Rheumatology and Clinical Immunology, Justus-Liebig-University Giessen, Campus Kerckhoff, 61231 Bad Nauheim, Germany.

出版信息

Int J Mol Sci. 2019 Aug 22;20(17):4091. doi: 10.3390/ijms20174091.

DOI:10.3390/ijms20174091
PMID:31443349
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6747092/
Abstract

Rheumatic diseases encompass a diverse group of chronic disorders that commonly affect musculoskeletal structures. Osteoarthritis (OA) and rheumatoid arthritis (RA) are the two most common, leading to considerable functional limitations and irreversible disability when patients are unsuccessfully treated. Although the specific causes of many rheumatic conditions remain unknown, it is generally accepted that immune mechanisms and/or uncontrolled inflammatory responses are involved in their etiology and symptomatology. In this regard, the bidirectional communication between neuroendocrine and immune system has been demonstrated to provide a homeostatic network that is involved in several pathological conditions. Adipokines represent a wide variety of bioactive, immune and inflammatory mediators mainly released by adipocytes that act as signal molecules in the neuroendocrine-immune interactions. Adipokines can also be synthesized by synoviocytes, osteoclasts, osteoblasts, chondrocytes and inflammatory cells in the joint microenvironment, showing potent modulatory properties on different effector cells in OA and RA pathogenesis. Effects of adiponectin, leptin, resistin and visfatin on local and systemic inflammation are broadly described. However, more recently, other adipokines, such as progranulin, chemerin, lipocalin-2, vaspin, omentin-1 and nesfatin, have been recognized to display immunomodulatory actions in rheumatic diseases. This review highlights the latest relevant findings on the role of the adipokine network in the pathophysiology of OA and RA.

摘要

风湿性疾病包括一组常见影响肌肉骨骼结构的慢性疾病。骨关节炎(OA)和类风湿关节炎(RA)是最常见的两种疾病,当患者治疗不成功时,会导致相当大的功能限制和不可逆转的残疾。尽管许多风湿性疾病的具体病因仍不清楚,但普遍认为免疫机制和/或不受控制的炎症反应参与了它们的病因和症状。在这方面,已经证明神经内分泌和免疫系统的双向通讯提供了一个参与多种病理状况的动态平衡网络。脂肪因子是主要由脂肪细胞释放的多种生物活性、免疫和炎症介质,作为神经内分泌-免疫相互作用中的信号分子。脂肪因子也可以由滑膜细胞、破骨细胞、成骨细胞、软骨细胞和关节微环境中的炎症细胞合成,在 OA 和 RA 发病机制中对不同的效应细胞具有强大的调节作用。脂肪因子如脂联素、瘦素、抵抗素和内脂素对局部和全身炎症的影响被广泛描述。然而,最近,其他脂肪因子,如颗粒蛋白前体、趋化素、脂联素-2、vaspin、网膜素-1 和 nesfatin,被认为在风湿性疾病中具有免疫调节作用。这篇综述强调了脂肪因子网络在 OA 和 RA 病理生理学中的最新相关研究结果。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a090/6747092/7e7b5d40af7f/ijms-20-04091-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a090/6747092/7e7b5d40af7f/ijms-20-04091-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a090/6747092/7e7b5d40af7f/ijms-20-04091-g001.jpg

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