RAGE deficiency obstructs high uric acid-induced oxidative stress and inflammatory response.

• Tác giả: Binyang Chen, Jidong Cheng, Furong He, Hidenori Koyama, Jiamin Lv, Qiang Wang, De Xie, Chenggui Zhang, Hairong Zhao
• Ngôn ngữ: eng
• Thông tin xuất bản: Netherlands : International immunopharmacology , 2025
• Bộ sưu tập: NCBI
• ID: 643434

Tóm tắt

Hyperuricemia is a metabolic disorder primarily associated with gout and implicated in various metabolic inflammatory diseases. While the role of monosodium urate crystals triggering inflammation has been well-documented, recent findings suggest that soluble high uric acid (HUA) also induces pro-inflammatory cytokine production in human monocytes. However, the comprehensive effects of HUA levels on macrophage dysfunction and the underlying mechanisms remain underexplored. This study employs urate oxidase knockout (UOX-KO) and receptor for advanced glycation end products deficiency (RAGE