The pathogenesis and regulatory role of HIF-1 in rheumatoid arthritis

IF 1.5 4区 医学 Q4 IMMUNOLOGY
Han Li, Qi-Yang Wu, Xu-Heng Teng, Zhi-Peng Li, Meng-Ting Zhu, Chao-Jie Gu, Ben-Jia Chen, Qi-Qi Xie, Xin-Jing Luo
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引用次数: 0

Abstract

Rheumatoid arthritis (RA) is a prevalent autoimmune disease that involves the overgrowth and inflammation of synovial tissue, leading to the degeneration and impairment of joints. In recent years, numerous studies have shown a close relationship between the hypoxic microenvironment in joints and the occurrence and progression of RA. The main cause of the pathological changes in RA is widely believed to be the abnormal expression of hypoxia-inducible factor-1 (HIF-1) in joints. This paper describes and illustrates the structure and primary functions of HIF-1 and explains the main regulatory methods of HIF-1, including the PHDs/HIF-1/pVHL pathway, factor-inhibiting HIF (FIH), regulation of inflammatory cytokines, and the NF-B pathway. Furthermore, this paper discusses the mechanism of HIF-1 and its impact on inflammation, angiogenesis, and cartilage destruction in greater detail. We summarize previous research findings on the mechanism of HIF-1 and propose new potential treatments for RA based on the pathogenesis of HIF-1 in RA.
类风湿性关节炎的发病机制和 HIF-1 的调节作用
类风湿性关节炎(RA)是一种常见的自身免疫性疾病,涉及滑膜组织的过度生长和炎症,导致关节退化和功能障碍。近年来,大量研究表明,关节缺氧微环境与 RA 的发生和发展密切相关。缺氧诱导因子-1(hypoxia-inducible factor-1,HIF-1)在关节中的异常表达被广泛认为是导致RA病理变化的主要原因。本文描述并说明了HIF-1的结构和主要功能,并解释了HIF-1的主要调控方法,包括PHDs/HIF-1/pVHL途径、抑制HIF的因子(FIH)、炎症细胞因子的调控以及NF-B途径。此外,本文还更详细地讨论了 HIF-1 的机制及其对炎症、血管生成和软骨破坏的影响。我们总结了以往关于HIF-1机制的研究成果,并根据HIF-1在RA中的发病机制提出了治疗RA的新方法。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
CiteScore
3.00
自引率
0.00%
发文量
17
审稿时长
6-12 weeks
期刊介绍: Central European Journal of Immunology is a English-language quarterly aimed mainly at immunologists.
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