ArticleThe Journal of biological chemistry2015
Rotenone-induced Impairment of Mitochondrial Electron Transport Chain Confers a Selective Priming Signal for NLRP3 Inflammasome Activation.
Article in The Journal of biological chemistry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 92 papers, 2 of them syntheses that pooled it.
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Who cites it
92 citing papers in PubMed, 2 syntheses or guidelines pooled it, 130 citations in OpenAlex.
- Beyond apoptosis: evidence of other regulated cell death pathways in the ovary throughout development and life.Human reproduction update · 2023Pooled it
- Pooled it
- Therapeutic potential of MitoQ, a mitochondria-targeted antioxidant, in age-related physiological dysfunction.GeroScience · 2026Review
- The Role of Skeletal Muscle Mitochondria in NLRP3 Inflammasome Signaling.Biomolecules · 2026Review
- Mitochondrial Metabolic Reprogramming and Skin Immune Homeostasis: From Basic Mechanisms to Therapeutic Perspectives.Immune network · 2026Review
- Inflammasome activation dictates the efficacy of antimycobacterial activity of frontline TB drugs.PLoS pathogens · 2026Article
- Phosphatidylinositol-3-kinase/Protein Kinase B (PI3K/AKT) and Nucleotide-Binding Oligomerization Domain-like Receptor Family Pyrin Domain Containing 3 (NLRP3) Inflammasome Modulation Underlies the Neuroprotective Effects of Vildagliptin in a Rotenone-Induced Mouse Model of Parkinson's Disease.ACS pharmacology & translational science · 2026Article
- Beyond Amyloids: Neuroprotective Potential of Betanin and its Derivatives Against Alpha-Synuclein Aggregates and ROS Overload in Parkinson's Disease.Journal of molecular neuroscience : MN · 2026Article
- Novel Non-Invasive PET Imaging of Reactive Oxygen Species Using [18 F]ROStrace in Three Proteinopathy-Associated Neurodegenerative Mouse Models.Academic radiology · 2026Article
- Chasteberry extract alleviates rotenone-triggered testicular injury in rats by modulating oxidative stress, inflammation, apoptosis, and mitochondrial dysfunction.Scientific reports · 2026Article
- Host mitochondrial DNA in bacterial pathogenesis: Friend, Foe, or Both?Archives of microbiology · 2026Review
- The succinate prodrug NV354 prevents brain lesions and late-stage motor dysfunction in mitochondrial complex I deficiency.iScience · 2026Article
- APOE4 impairs Nrf2-PINK1/Parkin-dependent mitochondrial clearance through disrupted antioxidant and mitophagy signaling.Free radical biology & medicine · 2026Article
- Tumor necrosis factor alpha triggers mitochondrial dysfunction and ROS-driven cytokine amplification in bovine fibroblast-like synoviocytes.Frontiers in veterinary science · 2026Article
- Article
- cGAS-STING-NF-κB Axis Mediates Rotenone-Induced NLRP3 Inflammasome Activation Through Mitochondrial DNA Release.Antioxidants (Basel, Switzerland) · 2025Article
- Mitochondrial DNA signals driving immune responses: Why, How, Where?Cell communication and signaling : CCS · 2025Review
- SomaticiScience · 2025Article
- Immune cell metabolic dysfunction in Parkinson's disease.Molecular neurodegeneration · 2025Review
- Evaluating the efficacy of vatiquinone in preclinical models of Leigh syndrome and GPX4 deficiency.Orphanet journal of rare diseases · 2025Article
32 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mitochondrial dysfunction is considered crucial for NLRP3 inflammasome activation partly through its release of mitochondrial toxic products, such as mitochondrial reactive oxygen species (mROS)(2) and mitochondrial DNA (mtDNA). Although previous studies have shown that classical NLRP3-activating stimulations lead to mROS generation and mtDNA release, it remains poorly understood whether and how mitochondrial damage-derived factors may contribute to NLRP3 inflammasome activation. Here, we demonstrate that impairment of the mitochondrial electron transport chain by rotenone primes NLRP3 inflammasome activation only upon costimulation with ATP and not with nigericin or alum. Rotenone-induced priming of NLRP3 in the presence of ATP triggered the formation of specklike NLRP3 or ASC aggregates and the association of NLRP3 with ASC, resulting in NLRP3-dependent caspase-1 activation. Mechanistically, rotenone confers a priming signal for NLRP3 inflammasome activation only in the context of aberrant high-grade, but not low-grade, mROS production and mitochondrial hyperpolarization. By contrast, rotenone/ATP-mediated mtDNA release and mitochondrial depolarization are likely to be merely an indication of mitochondrial damage rather than triggering factors for NLRP3 inflammasome activation. Our results provide a molecular insight into the selective contribution made by mitochondrial dysfunction to the NLRP3 inflammasome pathway.
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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.