ArticleNature immunology2022
Mitochondrial electron transport chain is necessary for NLRP3 inflammasome activation.
Article in Nature immunology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 203 papers, 2 of them syntheses that pooled it.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
203 citing papers in PubMed, 2 syntheses or guidelines pooled it, 312 citations in OpenAlex.
- The impact of post-translational modifications and subcellular localization on NLRP3 inflammasome activation: A systematic review.Cell communication and signaling : CCS · 2025Pooled it
- Systematic review ofFrontiers in aging neuroscience · 2023Pooled it
- Skin regeneration axis under metal-based nanozymes: from chronic wound healing to structural and functional restoration.Journal of advanced research · 2026Review
- Review
- Formation of tertiary lymphoid structures drives Parkin antitumor immunity.Science advances · 2026Article
- Mitochondrial electron transport chain is essential for acute inflammatory stress responses in mouse fibroblasts.Scientific reports · 2026Article
- Electrical Signals at the Subcellular Scale: How Electroactive Materials Regulate Stem Cell Fate.Advanced materials (Deerfield Beach, Fla.) · 2026Review
- Unveiling Gut Homeostasis Disruption in Sepsis: Towards an Integrated Mechanistic and Translational Roadmap.Cell proliferation · 2026Review
- The Role of Inflammation and Immunity in Cardiovascular Disease: Molecular Mechanisms and Therapeutic Targets.MedComm · 2026Review
- Article
- Research Progress on ROS Scavenging and Responsive Materials for Biomedical Applications.ACS omega · 2026Review
- Unleashing innovative cross-organ fibrosis therapies by harnessing the omics revolution.JCI insight · 2026Review
- Phase separation drives NLRP3 inflammasome activation independently of Golgi localization.Cell death & disease · 2026Article
- Decoding neuroinflammation: the critical role of NLRP3 inflammasome in Alzheimer's disease.Inflammopharmacology · 2026Review
- Statins promote muscle metabolic danger and NLRP3-mediated myopathy via lower protein-prenylation and YAP.Science advances · 2026Article
- The effect of Staphylococcus aureus targeting ROS-dependent mitochondrial damage activating NLRP10 in inducing skin and soft tissue infection.Scientific reports · 2026Article
- Mechanisms and disease relevance of mitochondrial translation in humans.Nature reviews. Molecular cell biology · 2026Review
- Skeletal Muscle Redox Signaling in Health and Disease: From Molecular Mechanisms to Therapeutic Exercise Strategies.Antioxidants (Basel, Switzerland) · 2026Review
- ROS breaks the cofilin lock on NLRP3.Nature immunology · 2026Article
- Glycerol enhances mitochondrial metabolism and inflammatory response in pro-inflammatory macrophages.EMBO reports · 2026Article
143 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
12 authors at 2 institutions in 4 countries.
Funding
Abstract
The NLRP3 inflammasome is linked to sterile and pathogen-dependent inflammation, and its dysregulation underlies many chronic diseases. Mitochondria have been implicated as regulators of the NLRP3 inflammasome through several mechanisms including generation of mitochondrial reactive oxygen species (ROS). Here, we report that mitochondrial electron transport chain (ETC) complex I, II, III and V inhibitors all prevent NLRP3 inflammasome activation. Ectopic expression of Saccharomyces cerevisiae NADH dehydrogenase (NDI1) or Ciona intestinalis alternative oxidase, which can complement the functional loss of mitochondrial complex I or III, respectively, without generation of ROS, rescued NLRP3 inflammasome activation in the absence of endogenous mitochondrial complex I or complex III function. Metabolomics revealed phosphocreatine (PCr), which can sustain ATP levels, as a common metabolite that is diminished by mitochondrial ETC inhibitors. PCr depletion decreased ATP levels and NLRP3 inflammasome activation. Thus, the mitochondrial ETC sustains NLRP3 inflammasome activation through PCr-dependent generation of ATP, but via a ROS-independent mechanism.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.