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Pyroptosis Plays a Role in Osteoarthritis

Authors
  • An, Senbo
  • Hu, Huiyu
  • Li, Yusheng
  • Hu, Yihe
Type
Published Article
Journal
Aging and Disease
Publisher
JKL International LLC
Publication Date
Oct 01, 2020
Volume
11
Issue
5
Pages
1146–1157
Identifiers
DOI: 10.14336/AD.2019.1127
PMID: 33014529
PMCID: PMC7505276
Source
PubMed Central
Keywords
License
Green

Abstract

Recent studies have revealed novel forms of cell death beyond the canonical types of cellular apoptosis and necrosis, and these novel forms of cell death are induced by extreme microenvironmental factors. Pyroptosis, a type of regulated cell death, occurs when pattern recognition receptors (PRRs) induce the activation of cysteine-aspartic protease 1 (caspase-1) or caspase-11, which can trigger the release of the pyrogenic cytokines interleukin-1β (IL-1β) and IL-18. Osteoarthritis (OA), the most common joint disease worldwide, is characterized by low-grade inflammation and increased levels of cytokines, including IL-1β and IL-18. Additionally, some damaged chondrocytes associated with OA exhibit morphological changes consistent with pyroptosis, suggesting that this form of regulated cell death may contribute significantly to the pathology of OA. This review summarizes the molecular mechanisms of pyroptosis and shows the critical role of NLRP3 (NLR family, pyrin domain containing 3; NLR refers to “nucleotide-binding domain, leucine-rich repeat”) inflammasomes. We also provide evidence describing potential role of pyroptosis in OA, including the relationship with OA risk factors and the contribution to cartilage degradation, synovitis and OA pain.

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