Frontiers in Immunology (Apr 2022)

Inflammatory Response to Regulated Cell Death in Gout and Its Functional Implications

  • Jianan Zhao,
  • Jianan Zhao,
  • Jianan Zhao,
  • Kai Wei,
  • Kai Wei,
  • Kai Wei,
  • Ping Jiang,
  • Ping Jiang,
  • Ping Jiang,
  • Cen Chang,
  • Cen Chang,
  • Cen Chang,
  • Lingxia Xu,
  • Lingxia Xu,
  • Lingxia Xu,
  • Linshuai Xu,
  • Linshuai Xu,
  • Linshuai Xu,
  • Yiming Shi,
  • Yiming Shi,
  • Yiming Shi,
  • Shicheng Guo,
  • Shicheng Guo,
  • Yu Xue,
  • Dongyi He,
  • Dongyi He,
  • Dongyi He,
  • Dongyi He

DOI
https://doi.org/10.3389/fimmu.2022.888306
Journal volume & issue
Vol. 13

Abstract

Read online

Gout, a chronic inflammatory arthritis disease, is characterized by hyperuricemia and caused by interactions between genetic, epigenetic, and metabolic factors. Acute gout symptoms are triggered by the inflammatory response to monosodium urate crystals, which is mediated by the innate immune system and immune cells (e.g., macrophages and neutrophils), the NACHT, LRR, and PYD domains-containing protein 3 (NLRP3) inflammasome activation, and pro-inflammatory cytokine (e.g., IL-1β) release. Recent studies have indicated that the multiple programmed cell death pathways involved in the inflammatory response include pyroptosis, NETosis, necroptosis, and apoptosis, which initiate inflammatory reactions. In this review, we explore the correlation and interactions among these factors and their roles in the pathogenesis of gout to provide future research directions and possibilities for identifying potential novel therapeutic targets and enhancing our understanding of gout pathogenesis.

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