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软骨与骨破坏的分子生物学

Molecular biology of cartilage and bone destruction.

作者信息

Müller-Ladner U, Gay R E, Gay S

机构信息

Department of Internal Medicine I, University of Regensburg, Germany.

出版信息

Curr Opin Rheumatol. 1998 May;10(3):212-9. doi: 10.1097/00002281-199805000-00010.

DOI:10.1097/00002281-199805000-00010
PMID:9608324
Abstract

Molecular biology has provided various new insights into the mechanisms operative in the pathogenesis of rheumatoid arthritis. Reflecting the unique character of rheumatoid synovium, advances have been achieved addressing the molecular changes taking place at the area of interaction between the aggressively growing synovium and the articular cartilage and bone. Key issues in the review period addressing this interaction were hyperplasia of rheumatoid arthritis synovium, mechanisms of activation and cell cycle regulation of synovial fibroblasts, pathways of synovial attachment to cartilage and bone, and the regulation of matrix-degrading enzymes.

摘要

分子生物学为类风湿关节炎发病机制中的作用机制提供了各种新见解。鉴于类风湿滑膜的独特性质,在侵袭性生长的滑膜与关节软骨和骨之间相互作用区域发生的分子变化方面已取得进展。在本综述期间,针对这种相互作用的关键问题包括类风湿关节炎滑膜增生、滑膜成纤维细胞的激活机制和细胞周期调控、滑膜与软骨和骨的附着途径以及基质降解酶的调控。

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Molecular biology of cartilage and bone destruction.软骨与骨破坏的分子生物学
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["Rheumatism"--pathophysiologic principles].["风湿病"——病理生理原理]
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Early structural changes in cartilage and bone are required for the attachment and invasion of inflamed synovial tissue during destructive inflammatory arthritis.早期的软骨和骨结构变化是炎症性关节炎破坏性过程中附着和侵犯炎症滑膜组织所必需的。
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Mechanism of joint destruction in rheumatoid arthritis.类风湿关节炎中关节破坏的机制。
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Deficiency of fibroblast activation protein alpha ameliorates cartilage destruction in inflammatory destructive arthritis.成纤维细胞活化蛋白α缺乏可改善炎性破坏性关节炎中的软骨破坏。
Arthritis Res Ther. 2015 Jan 20;17(1):12. doi: 10.1186/s13075-015-0524-6.
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Cell culture and passaging alters gene expression pattern and proliferation rate in rheumatoid arthritis synovial fibroblasts.
细胞培养和传代会改变类风湿关节炎滑膜成纤维细胞的基因表达模式和增殖速度。
Arthritis Res Ther. 2010;12(3):R83. doi: 10.1186/ar3010. Epub 2010 May 12.
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Discrepancy between mRNA and protein expression of tumour suppressor maspin in synovial tissue may contribute to synovial hyperplasia in rheumatoid arthritis.滑膜组织中肿瘤抑制因子maspin的mRNA与蛋白质表达之间的差异可能导致类风湿关节炎中的滑膜增生。
Ann Rheum Dis. 2004 Oct;63(10):1205-11. doi: 10.1136/ard.2003.006312.
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Proposal for a sonographic classification of target joints in rheumatoid arthritis.
Rheumatol Int. 2005 Apr;25(3):215-9. doi: 10.1007/s00296-003-0418-9. Epub 2003 Dec 5.
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The ICIDH-2 as a framework for the assessment of functioning and disability in rheumatoid arthritis.《国际功能、残疾和健康分类(第二版)》作为类风湿性关节炎功能和残疾评估的框架。
Ann Rheum Dis. 2002 Mar;61(3):225-31. doi: 10.1136/ard.61.3.225.
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Cathepsin k is a critical protease in synovial fibroblast-mediated collagen degradation.组织蛋白酶K是滑膜成纤维细胞介导的胶原蛋白降解中的一种关键蛋白酶。
Am J Pathol. 2001 Dec;159(6):2167-77. doi: 10.1016/S0002-9440(10)63068-4.
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Kinesin-like protein CENP-E is upregulated in rheumatoid synovial fibroblasts.驱动蛋白样蛋白CENP - E在类风湿性滑膜成纤维细胞中上调。
Arthritis Res. 1999;1(1):71-80. doi: 10.1186/ar13. Epub 1999 Oct 26.
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IL-4 gene therapy for collagen arthritis suppresses synovial IL-17 and osteoprotegerin ligand and prevents bone erosion.用于胶原性关节炎的白细胞介素-4基因疗法可抑制滑膜白细胞介素-17和骨保护素配体,并防止骨质侵蚀。
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