Mitochondria and NLRP3: To die or inflame

Shuangshuang Yang; Guannan Huang; Jenny P-Y Ting

doi:10.1016/j.immuni.2024.12.007

Mitochondria and NLRP3: To die or inflame

Immunity. 2025 Jan 14;58(1):5-7. doi: 10.1016/j.immuni.2024.12.007.

Authors

Shuangshuang Yang¹, Guannan Huang¹, Jenny P-Y Ting²

Affiliations

¹ Department of Genetics, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA; Lineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA; Department of Microbiology and Immunology, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA.
² Department of Genetics, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA; Lineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA; Department of Microbiology and Immunology, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA. Electronic address: [email protected].

PMID: 39813994
DOI: 10.1016/j.immuni.2024.12.007

Abstract

Mitochondria play critical roles in intrinsic apoptosis and NLRP3 inflammasome activation, but how these processes are interconnected remains unclear. In this issue of Immunity, Saller et al. unveiled the complexity of NLRP3 activators, highlighting mitochondria's roles in switching apoptosis to NLRP3 inflammasome activation.

Publication types

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MeSH terms

Animals
Apoptosis* / immunology
Humans
Inflammasomes* / immunology
Inflammasomes* / metabolism
Mitochondria* / metabolism
NLR Family, Pyrin Domain-Containing 3 Protein* / metabolism

Substances

NLR Family, Pyrin Domain-Containing 3 Protein
Inflammasomes