Journal
CELLS
Volume 11, Issue 8, Pages -Publisher
MDPI
DOI: 10.3390/cells11081307
Keywords
inflammation; pyroptosis; inflammasomes; gasdermins; rheumatoid arthritis; fibroblast-macrophage cross-talk; TAM receptors
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Funding
- European Molecular Biology Organization (EMBO) [ALTF 108-2021]
- Kennedy Trust, KTRR start-up fellowship [KENN 15 16 06]
- MRC [MR/W001217/1, MR/S000623/1]
- Kennedy Trust, KTPS Studentships
- MRC [MR/S000623/1] Funding Source: UKRI
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This review discusses the impact of pyroptosis on tissue damage and inflammation, with a particular focus on injury-induced and autoimmune arthritis. Gasdermins, the executors of pyroptosis, play an important role in regulating cell death by forming pores at the plasma membrane.
About thirty years ago, a new form of pro-inflammatory lytic cell death was observed and termed pyroptosis. Only in 2015, gasdermins were defined as molecules that create pores at the plasma membrane and drive pyroptosis. Today, we know that gasdermin-mediated death is an important antimicrobial defence mechanism in bacteria, yeast and mammals as it destroys the intracellular niche for pathogen replication. However, excessive and uncontrolled cell death also contributes to immunopathology in several chronic inflammatory diseases, including arthritis. In this review, we discuss recent findings where pyroptosis contributes to tissue damage and inflammation with a main focus on injury-induced and autoimmune arthritis. We also review novel functions and regulatory mechanisms of the pyroptotic executors gasdermins. Finally, we discuss possible models of how pyroptosis may contribute to the cross-talk between fibroblast and macrophages, and also how this cross-talk may regulate inflammation by modulating inflammasome activation and pyroptosis induction.
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