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The pathogenesis and regulatory role of HIF-1 in rheumatoid arthritis.
Li, Han; Wu, Qi-Yang; Teng, Xu-Heng; Li, Zhi-Peng; Zhu, Meng-Ting; Gu, Chao-Jie; Chen, Ben-Jia; Xie, Qi-Qi; LuO, Xin-Jing.
Afiliação
  • Li H; Taizhou University, Taizhou, Zhejiang, China.
  • Wu QY; Taizhou University, Taizhou, Zhejiang, China.
  • Teng XH; Taizhou University, Taizhou, Zhejiang, China.
  • Li ZP; Taizhou University, Taizhou, Zhejiang, China.
  • Zhu MT; Taizhou University, Taizhou, Zhejiang, China.
  • Gu CJ; Taizhou University, Taizhou, Zhejiang, China.
  • Chen BJ; Taizhou University, Taizhou, Zhejiang, China.
  • Xie QQ; Taizhou University, Taizhou, Zhejiang, China.
  • LuO XJ; Taizhou University, Taizhou, Zhejiang, China.
Cent Eur J Immunol ; 48(4): 338-345, 2023.
Article em En | MEDLINE | ID: mdl-38558567
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 α/pVHL pathway, factor-inhibiting HIF (FIH), regulation of inflammatory cytokines, and the NF-κB 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.
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Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Idioma: En Revista: Cent Eur J Immunol Ano de publicação: 2023 Tipo de documento: Article País de afiliação: China

Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Idioma: En Revista: Cent Eur J Immunol Ano de publicação: 2023 Tipo de documento: Article País de afiliação: China