ArticleProceedings of the National Academy of Sciences of the United States of America2012
Critical role for calcium mobilization in activation of the NLRP3 inflammasome.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 541 papers.
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Who cites it
541 citing papers in PubMed, 891 citations in OpenAlex.
- Unmasking programmed cell death in rhinovirus-driven asthma pathology.Biochemical Society transactions · 2026Review
- From mitochondria to innate immunity: The mtDNA-driven cGAS/STING-NLRP3 cascade and its therapeutic implications in neurodegenerative diseases (Review).Experimental and therapeutic medicine · 2026Review
- The NLRP3 inflammasome at the crossroads of innate immune signaling and cell death.Cellular & molecular immunology · 2026Review
- Redefining the Evolution of Pulpal Pathology: Inflammasomes as Central Integrative Hubs and Biological Switches Governing the Transition From Reversible to Irreversible Pulpal Inflammation Beyond Symptom-Based Classification.International endodontic journal · 2026Review
- Targeting Gasdermins for Therapeutic Interventions in Central Nervous System Injury.Neurotoxicity research · 2026Review
- The Role of Skeletal Muscle Mitochondria in NLRP3 Inflammasome Signaling.Biomolecules · 2026Review
- Comorbidities and Inflammation: How Chronic Diseases Prime the Host Response in Sepsis.International journal of molecular sciences · 2026Review
- A Review on Structural Insights into NLRP3 and NEK7: Domain Architecture, Subcellular Localization, and Their Interaction in Inflammasome Assembly and Signaling.Molecular neurobiology · 2026Review
- Mitochondrial Metabolic Reprogramming and Skin Immune Homeostasis: From Basic Mechanisms to Therapeutic Perspectives.Immune network · 2026Review
- Transient receptor potential vanilloid channels in inflammatory bowel diseases: linking inflammation, angiogenesis, and oxidative stress.Inflammopharmacology · 2026Review
- Deconstructing the Master Switch: Advances in Direct NLRP3 Inhibition.Pharmaceuticals (Basel, Switzerland) · 2026Review
- Potential link between Gordonibacter pamelaeae and phospholipase C gamma 1 in osteoarthritis.AMB Express · 2026Article
- Potential mechanisms of natural products in improving gouty arthritis: Focusing on NLRP3 inflammasome regulation.Journal of pharmaceutical analysis · 2026Review
- Piezo1 Activation by Shear Stress Induces Corneal Epithelial Homeostasis Disruption.Investigative ophthalmology & visual science · 2026Article
- Inflammatory Biomarkers and Their Associations with Arrhythmic Burden Following SGLT2-I Treatment in Chronic Heart Failure-A Subanalysis of the ERASe Trial.Journal of clinical medicine · 2026Article
- A pH-responsive layered double hydroxide nanoradiosensitizer for bone metastasis tumor.Materials today. Bio · 2026Article
- An "old" cytokine's new trick: IL-1β in B cells and the germinal center.Function (Oxford, England) · 2026Review
- NLRP3 inflammasome promotes PAD2/PAD4 release and protein citrullination in rheumatoid arthritis.Communications biology · 2026Article
- Plasma SERPINA3 and its clinical correlates in adolescent major depressive disorder: an exploratory case-control study.BMC psychiatry · 2026Article
- Infectious bronchitis virus accessory protein 3a induces renal inflammatory injury by activating the NLRP3 inflammasome via ER calcium mobilization and mitochondrial ROS production.Journal of virology · 2026Article
481 more citing papers are in PubMed but not listed here.
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The NLRP3 (nucleotide-binding domain, leucine-rich-repeat-containing family, pyrin domain-containing 3) inflammasome mediates production of inflammatory mediators, such as IL-1β and IL-18, and as such is implicated in a variety of inflammatory processes, including infection, sepsis, autoinflammatory diseases, and metabolic diseases. The proximal steps in NLRP3 inflammasome activation are not well understood. Here we elucidate a critical role for Ca(2+) mobilization in activation of the NLRP3 inflammasome by multiple stimuli. We demonstrate that blocking Ca(2+) mobilization inhibits assembly and activation of the NLRP3 inflammasome complex, and that during ATP stimulation Ca(2+) signaling is pivotal in promoting mitochondrial damage. C/EPB homologous protein, a transcription factor that can modulate Ca(2+) release from the endoplasmic reticulum, amplifies NLRP3 inflammasome activation, thus linking endoplasmic reticulum stress to activation of the NLRP3 inflammasome. Our findings support a model for NLRP3 inflammasome activation by Ca(2+)-mediated mitochondrial damage.
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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.