ArticleCell communication and signaling : CCS2019
NFAT5 mediates hypertonic stress-induced atherosclerosis via activating NLRP3 inflammasome in endothelium.
Article in Cell communication and signaling : CCS, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 52 citations in OpenAlex.
- The NLRP3 Inflammasome: Mechanisms of Activation, Regulation, and Therapeutic Opportunities.MedComm · 2026Review
- The miR-1260b-NFAT5 axis regulates inflammasome priming and M1 macrophage polarization in periodontitis.Frontiers in immunology · 2026Article
- Inflammasomes and pyroptosis in cancer: mechanisms and therapeutic advances.Journal of hematology & oncology · 2025Review
- Microglial NFAT5 aggravates neuroinflammation via mediating NLRP6 inflammasome in experimental ischemic stroke.Genes & diseases · 2025Article
- Maternal Aspartame Exposure Induces Neonatal Pulmonary Metabolic Dysregulation and Redox Imbalance: A Multiomics Investigation of Gut Microbiota-Host Interactions.Journal of agricultural and food chemistry · 2025Article
- NEP1-40 Regulates the Development of Hippocampal Neural Stem Cells in Schizophrenic Mice.Current medical science · 2025Article
- Updated insights into the molecular networks for NLRP3 inflammasome activation.Cellular & molecular immunology · 2025Review
- NFAT5 exacerbates β-cell ferroptosis by suppressing the transcription of PRDX2 in obese type 2 diabetes mellitus.Cellular and molecular life sciences : CMLS · 2025Article
- NFAT5: a stress-related transcription factor with multiple functions in health and disease.Cell stress · 2025Review
- Discovery of KDM5D as a novel biomarker for traumatic brain injury identified through bioinformatics analysis.Frontiers in immunology · 2025Article
- Role of LncRNA in Trauma Susceptibility and Resilience to Post-Traumatic Stress Disorder (PTSD): A Pilot Study in the African American Population.Neuropsychiatric disease and treatment · 2025Article
- Inflammasome Molecular Insights in Autoimmune Diseases.Current issues in molecular biology · 2024Review
- Inhibition of NFAT5-Dependent Astrocyte Swelling Alleviates Neuropathic Pain.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- TonEBP: A Key Transcription Factor in Microglia Following Intracerebral Hemorrhage Induced-Neuroinflammation.International journal of molecular sciences · 2024Article
- Canonical and non-canonical functions of NLRP3.Journal of advanced research · 2023Review
- High Salt Promotes Inflammatory and Fibrotic Response in Peritoneal Cells.International journal of molecular sciences · 2023Article
- The NLRP3 inflammasome: contributions to inflammation-related diseases.Cellular & molecular biology letters · 2023Review
- Neutral amino acid transporter SLC38A2 protects renal medulla from hyperosmolarity-induced ferroptosis.eLife · 2023Article
- Circular RNAs to predict clinical outcome after cardiac arrest.Intensive care medicine experimental · 2022Article
- Role of NLRP3 inflammasome in systemic sclerosis.Arthritis research & therapy · 2022Review
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundHow high-salt intake leads to the occurrence of many cardiovascular diseases such as atherosclerosis is a fundamental question in pathology. Here we postulated that high-salt-induced NFAT5 controls the inflammasome activation by directly regulating NLRP3, which mediates the expression of inflammatory- and adhesion-related genes in vascular endothelium, resulting in the formation of atherosclerosis.
methodsAtherosclerosis-prone apolipoprotein E-deficient (ApoE-/-) mice which accumulate cholesterol ester-enriched particles in the blood due to poor lipoprotein clearance capacity were used as the atherosclerosis model in vivo. Cultured endothelial cells (ECs) and monocytes under high-salt condition were used to explore the atheroprone role of the activation of NFAT5-NLRP3 inflammasome in vascular endothelium in vitro. Bioinformatic analysis and chromatin immunoprecipitation assay were used to identify the DNA binding sites of NFAT5 on promoters of NLRP3 and IL-1β.
resultsWe first observe that high-salt intake promotes atherosclerosis formation in the aortas of ApoE
conclusionsOur study identifies NFAT5 as a new and essential transcription factor that is required for the early activation of NLRP3-inflammasome-mediated endothelium innate immunity, contributing to the formation of atherosclerosis under hypertonic stress induction.
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