ArticleEuropean heart journal2021
Macrophage NFATc3 prevents foam cell formation and atherosclerosis: evidence and mechanisms.
Article in European heart journal, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.
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Who cites it
54 citing papers in PubMed, 107 citations in OpenAlex.
- Impact of established cardiovascular disease on 10-year death after coronary revascularization for complex coronary artery disease.Clinical research in cardiology : official journal of the German Cardiac Society · 2021Trial
- MicroRNAs as master regulators of macrophage function in atherosclerosis: From polarization to therapeutic potential.iScience · 2026Review
- Study on the pro-inflammatory mechanism mediated by the RANK-SPP1 axis in macrophage immunomodulation during atherosclerosis.Molecular and cellular biochemistry · 2026Article
- PDK4 drives abdominal aortic aneurysm by promoting smooth muscle cell metabolic reprogramming and NLRP3-mediated pyroptosis.Nature communications · 2026Article
- DNA Methylation: A Key Epigenetic Regulator of Cardiovascular Diseases.Reviews in cardiovascular medicine · 2026Review
- Slc7a11-Mediated Cystine/Glutamate Antiport Reprograms Macrophage Polarization and Ameliorates Atherosclerosis.MedComm · 2026Article
- Multi-omics characterization of anoikis-related hub genes and macrophage-centered immune persistence with validation of HAVCR2 in atherosclerosis.Frontiers in immunology · 2026Article
- Biomaterials Promote the Regression of Atherosclerotic Plaque by Regulating Cell Behavior.International journal of nanomedicine · 2026Review
- Bibliometric analysis of research hotspots and emerging trends in microRNAs and atherosclerosis (2007-2025).Frontiers in cardiovascular medicine · 2026Review
- Research progress on macrophage regulation of atherosclerosis.Frontiers in cardiovascular medicine · 2026Review
- TLR2, CCR1, IRF8, and CCL4 as biomarkers for atherosclerosis progression and therapy response: A multi-omics study.Medicine · 2025Article
- Folate-modified biomimetic nanovesicles loaded with a PU.1 inhibitor alleviate atherosclerosis by suppressing inflammation.Journal of nanobiotechnology · 2025Article
- Oral targeting tilianin nanoplatform mitigates atherosclerosis through promoting macrophage phagocytosis and anti-inflammation.Materials today. Bio · 2025Article
- Pyruvate Carboxylase in Macrophages Aggravates Atherosclerosis by Regulating Metabolism Reprogramming to Promote Inflammatory Responses Through the Hypoxia-Inducible Factor-1 Signaling Pathway.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Cytoplasmic and nuclear NFATc3 cooperatively contributes to vascular smooth muscle cell dysfunction and drives aortic aneurysm and dissection.Acta pharmaceutica Sinica. B · 2025Article
- The molecular mechanism by which CTSB degrades FPN to disrupt macrophage iron homeostasis and promote the progression of atherosclerosis.Molecular and cellular biochemistry · 2025Article
- Vascular Smooth Muscle Cells: A Therapeutic Target in Atherosclerosis.Reviews in cardiovascular medicine · 2025Review
- Macrophage HM13/SPP Enhances Foamy Macrophage Formation and Atherogenesis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Dysregulated cholesterol uptake and efflux of bone marrow-derived α-SMACellular and molecular life sciences : CMLS · 2025Article
- Bioinformatics analysis to investigate the potential relationship between mitochondrial structure and function-related genes and the immune microenvironment in atherosclerosis.Frontiers in cardiovascular medicine · 2025Article
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Authors and funding
21 authors at 6 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimsOur previous study demonstrated that Ca2+ influx through the Orai1 store-operated Ca2+ channel in macrophages contributes to foam cell formation and atherosclerosis via the calcineurin-ASK1 pathway, not the classical calcineurin-nuclear factor of activated T-cell (NFAT) pathway. Moreover, up-regulation of NFATc3 in macrophages inhibits foam cell formation, suggesting that macrophage NFATc3 is a negative regulator of atherogenesis. Hence, this study investigated the precise role of macrophage NFATc3 in atherogenesis. METHODS AND
resultsMacrophage-specific NFATc3 knockout mice were generated to determine the effect of NFATc3 on atherosclerosis in a mouse model of adeno-associated virus-mutant PCSK9-induced atherosclerosis. NFATc3 expression was decreased in macrophages within human and mouse atherosclerotic lesions. Moreover, NFATc3 levels in peripheral blood mononuclear cells from atherosclerotic patients were negatively associated with plaque instability. Furthermore, macrophage-specific ablation of NFATc3 in mice led to the atherosclerotic plaque formation, whereas macrophage-specific NFATc3 transgenic mice exhibited the opposite phenotype. NFATc3 deficiency in macrophages promoted foam cell formation by potentiating SR-A- and CD36-meditated lipid uptake. NFATc3 directly targeted and transcriptionally up-regulated miR-204 levels. Mature miR-204-5p suppressed SR-A expression via canonical regulation. Unexpectedly, miR-204-3p localized in the nucleus and inhibited CD36 transcription. Restoration of miR-204 abolished the proatherogenic phenotype observed in the macrophage-specific NFATc3 knockout mice, and blockade of miR-204 function reversed the beneficial effects of NFATc3 in macrophages.
conclusionMacrophage NFATc3 up-regulates miR-204 to reduce SR-A and CD36 levels, thereby preventing foam cell formation and atherosclerosis, indicating that the NFATc3/miR-204 axis may be a potential therapeutic target against atherosclerosis.
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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.