Suppr超能文献

假设:人类关节炎中的软骨分解代谢辅助因子。

Hypothesis: cartilage catabolic cofactors in human arthritis.

作者信息

Hollander A P, Dieppe P A, Atkins R M, Elson C J

机构信息

Joint Diseases Laboratory, Shriners Hospital for Crippled Children, Montreal, PQ, Canada.

出版信息

J Rheumatol. 1993 Feb;20(2):223-4.

PMID:8474056
Abstract

Cartilage degradation in rheumatoid arthritis (RA) and osteoarthritis (OA) is commonly thought to be mediated by interleukin 1 (IL-1) and tumor necrosis factor (TNF). However, recent new evidence suggests that IL-1 and TNF on their own do not mediate all the cartilage changes seen in RA and OA. We propose that cartilage degradation is mediated by a complex network of cytokines, including IL-1, TNF and at least one cofactor present in synovial fluid.

摘要

类风湿性关节炎(RA)和骨关节炎(OA)中的软骨降解通常被认为是由白细胞介素1(IL-1)和肿瘤坏死因子(TNF)介导的。然而,最近的新证据表明,IL-1和TNF自身并不能介导RA和OA中出现的所有软骨变化。我们提出,软骨降解是由一个复杂的细胞因子网络介导的,包括IL-1、TNF以及滑液中存在的至少一种辅助因子。

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验