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Frontiers in immunology
2022;13 888306.

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

Jianan Zhao, Kai Wei, Ping Jiang, Cen Chang, Lingxia Xu, Linshuai Xu, Yiming Shi, Shicheng Guo, Yu Xue, Dongyi He
Author Information
  1. Jianan Zhao: Guanghua Clinical Medical College, Shanghai University of Traditional Chinese Medicine, Shanghai, China.
  2. Kai Wei: Guanghua Clinical Medical College, Shanghai University of Traditional Chinese Medicine, Shanghai, China.
  3. Ping Jiang: Guanghua Clinical Medical College, Shanghai University of Traditional Chinese Medicine, Shanghai, China.
  4. Cen Chang: Guanghua Clinical Medical College, Shanghai University of Traditional Chinese Medicine, Shanghai, China.
  5. Lingxia Xu: Guanghua Clinical Medical College, Shanghai University of Traditional Chinese Medicine, Shanghai, China.
  6. Linshuai Xu: Guanghua Clinical Medical College, Shanghai University of Traditional Chinese Medicine, Shanghai, China.
  7. Yiming Shi: Guanghua Clinical Medical College, Shanghai University of Traditional Chinese Medicine, Shanghai, China.
  8. Shicheng Guo: Computation and Informatics in Biology and Medicine, University of Wisconsin-Madison, Madison, WI, United States.
  9. Yu Xue: Department of Rheumatology, Huashan Hospital, Institute of Rheumatology, Immunology and Allergy, Fudan University, Shanghai, China.
  10. Dongyi He: Guanghua Clinical Medical College, Shanghai University of Traditional Chinese Medicine, Shanghai, China.
PMID: 35464445 DOI: 10.3389/fimmu.2022.888306

Abstract

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.

Keywords

NETosis apoptosis gout inflammation necroptosis programmed cell death pyroptosis

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MeSH Term

Arthritis, Gouty
Gout
Humans
Inflammasomes
Macrophages
Pyroptosis

Chemicals

Inflammasomes
Journal Article Review Research Support, Non-U.S. Gov't
Article has an altmetric score of 1

Word Cloud

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