ArticleCell death & disease2015
K(+) regulates Ca(2+) to drive inflammasome signaling: dynamic visualization of ion flux in live cells.
Article in Cell death & disease, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 110 papers, 1 of them a synthesis that pooled it.
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Who cites it
110 citing papers in PubMed, 1 synthesis or guideline pooled it, 207 citations in OpenAlex.
- Systematic Overview of Solid Particles and Their Host Responses.Frontiers in immunology · 2018Pooled it
- Advances in calcium signalling research for the diagnosis and treatment of depression.Annals of medicine · 2026Review
- The NLRP3 inflammasome at the crossroads of innate immune signaling and cell death.Cellular & molecular immunology · 2026Review
- Porcine coronavirus promotes NLRP3 inflammasome activation during virus-induced neuroinflammation.mBio · 2026Article
- Cardiovascular Imaging for the Early Detection of Cardiotoxicity from Emerging Cancer Therapies: Mechanistic Insights Across the Pediatric and Adult Spectrum.Journal of personalized medicine · 2026Review
- Time-lapse image analysis reveals trigger-dependent differences in ASC speck lifetime in the NLRP3 inflammasome.Scientific reports · 2026Article
- P2X7 receptor: a potential therapeutic target for chronic respiratory diseases.Molecular and cellular biochemistry · 2026Review
- The P2X7 Receptor Promotes Intestinal Fibrosis by Modulating the Gut Microbiota and the Inflammasome.Cellular and molecular gastroenterology and hepatology · 2026Article
- VNUT-mediated ATP release suppresses T helper 1 (TScience advances · 2025Article
- Radiation meets inflammation: NLRP3 inflammasome at the core of radiation-induced cardiac injury.Journal of translational medicine · 2025Review
- Biopolymer Membranes for Osmotic Power Generation in Bionic Applications.Advanced materials (Deerfield Beach, Fla.) · 2025Review
- Updated insights into the molecular networks for NLRP3 inflammasome activation.Cellular & molecular immunology · 2025Review
- Estrogen receptor β activation alleviates inflammatory bowel disease by suppressing NLRP3-dependent IL-1β production in macrophages via downregulation of intracellular calcium level.Journal of advanced research · 2025Article
- Role of Pannexin 1, P2X7, and CFTR in ATP Release and Autocrine Signaling by Principal Cells of the Epididymis.Function (Oxford, England) · 2025Article
- Radiotherapy elicits immunogenic cell death and metabolic shifts in the tumor microenvironment: implications for immunotherapy.International journal of medical sciences · 2025Review
- Coordination of innate immune responses by connexins.Frontiers in immunology · 2025Review
- NLRP3 Inflammasome Activation in Liver Disorders: From Molecular Pathways to Therapeutic Strategies.Journal of inflammation research · 2025Review
- Giant panda seasonal adaptations in feeding strategies and blood physiology.Frontiers in veterinary science · 2025Article
- NLRP3 and beyond: inflammasomes as central cellular hub and emerging therapeutic target in inflammation and disease.Frontiers in immunology · 2025Review
- Mechanistic Relevance of Ventricular Arrhythmias in Heart Failure with Preserved Ejection Fraction.International journal of molecular sciences · 2024Review
50 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
Abstract
P2X7 purinergic receptor engagement with extracellular ATP induces transmembrane potassium and calcium flux resulting in assembly of the NLRP3 inflammasome in LPS-primed macrophages. The role of potassium and calcium in inflammasome regulation is not well understood, largely due to limitations in existing methods for interrogating potassium in real time. The use of KS6, a novel sensor for selective and sensitive dynamic visualization of intracellular potassium flux in live cells, multiplexed with the intracellular calcium sensor Fluo-4, revealed a coordinated relationship between potassium and calcium. Interestingly, the mitochondrial potassium pool was mobilized in a P2X7 signaling, and ATP dose-dependent manner, suggesting a role for mitochondrial sensing of cytosolic ion perturbation. Through treatment with extracellular potassium we found that potassium efflux was necessary to permit sustained calcium entry, but not transient calcium flux from intracellular stores. Further, intracellular calcium chelation with BAPTA-AM indicated that P2X7-induced potassium depletion was independent of calcium mobilization. This evidence suggests that both potassium efflux and calcium influx are necessary for mitochondrial reactive oxygen generation upstream of NLRP3 inflammasome assembly and pyroptotic cell death. We propose a model wherein potassium efflux is necessary for calcium influx, resulting in mitochondrial reactive oxygen generation to trigger the NLRP3 inflammasome.
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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.