ArticleInternational journal of molecular sciences2015
miR-223 Inhibits Lipid Deposition and Inflammation by Suppressing Toll-Like Receptor 4 Signaling in Macrophages.
Article in International journal of molecular sciences, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers, 2 of them syntheses that pooled it.
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Who cites it
58 citing papers in PubMed, 2 syntheses or guidelines pooled it, 101 citations in OpenAlex.
- Using molecular methods to diagnose, classify, and treat neonatal sepsis: a scoping review.Frontiers in pediatrics · 2025Pooled it
- The Role of microRNAs in Pulp Inflammation.Cells · 2021Pooled it
- Unifying and unique roles of non-coding RNA biomarkers in liver and heart fibrosis.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2026Review
- MicroRNAs as master regulators of macrophage function in atherosclerosis: From polarization to therapeutic potential.iScience · 2026Review
- Review
- miR-223-3p improves macrophage polarization balance and mitochondrial metabolism to ameliorate uveitis by orchestrating P65Cellular & molecular biology letters · 2026Article
- Article
- Macrophage polarization in ischemia-reperfusion injury: from molecular mechanisms to therapeutic strategies.Frontiers in immunology · 2026Review
- Advances in the Regulation of Lipid Metabolism by Non-Coding RNAs.Animals : an open access journal from MDPI · 2025Review
- MicroRNA 223 Enhances ABCA1 Protein Stability and Supports Efflux in Cholesterol-Burdened Macrophages.Cell biochemistry and biophysics · 2025Article
- Preliminary Study of Differential circRNA Expression and Investigation of circRNA-miRNA-mRNA Competitive Endogenous Network in Rumen Acidosis of Holstein Cattle.Animals : an open access journal from MDPI · 2025Article
- Fraxin Alleviates Atherosclerosis by Inhibiting Oxidative Stress and Inflammatory Responses via the TLR4/PI3K/Akt Pathway.Current issues in molecular biology · 2025Article
- The Role of MicroRNA in the Pathophysiology and Diagnosis of Viral Myocarditis.International journal of molecular sciences · 2024Review
- MiR-223-3p in Cancer Development and Cancer Drug Resistance: Same Coin, Different Faces.International journal of molecular sciences · 2024Review
- MiR-223 enhances lipophagy by suppressing CTSB in microglia following lysolecithin-induced demyelination in mice.Lipids in health and disease · 2024Article
- MicroRNA-mediated metabolic regulation of immune cells in cancer: an updated review.Frontiers in immunology · 2024Review
- microRNA-223 and microRNA-126 are clinical indicators for predicting the plaque stability in carotid atherosclerosis patients.Journal of human hypertension · 2023Article
- Uremic Toxins Induce THP-1 Monocyte Endothelial Adhesion and Migration through Specific miRNA Expression.International journal of molecular sciences · 2023Article
- Transplantation of Exercise-Induced Extracellular Vesicles as a Promising Therapeutic Approach in Ischemic Stroke.Translational stroke research · 2023Review
- microRNAs Associated with Carotid Plaque Development and Vulnerability: The Clinician's Perspective.International journal of molecular sciences · 2022Review
Corrections and comments
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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
Atherosclerosis and its complications rank as the leading cause of death with the hallmarks of lipid deposition and inflammatory response. MicroRNAs (miRNAs) have recently garnered increasing interests in cardiovascular disease. In this study, we investigated the function of miR-223 and the underlying mechanism in atherosclerosis. In the atherosclerotic ApoE-/- mice models, an obvious increase of miR-223 was observed in aortic atherosclerotic lesions. In lipopolysaccharide (LPS) activated macrophages, its expression was decreased. The miR-223 overexpression significantly attenuated macrophage foam cell formation, lipid accumulation and pro-inflammatory cytokine production, which were reversed by anti-miR-223 inhibitor transfection. Mechanism assay corroborated that miR-223 negatively regulated the activation of the toll-like receptor 4 (TLR4)-nuclear factor-κB (NF-κB) pathway. Pretreatment with a specific inhibitor of NF-κB (pyrrolidinedithiocarbamate, PDTC) strikingly abrogated miR-223 silence-induced lipid deposition and inflammatory cytokine production. Furthermore, PI3K/AKT was activated by miR-223 up-regulation. Pretreatment with PI3K/AKT inhibitor LY294002 strikingly ameliorated the inhibitory effects of miR-223 on the activation of TLR4 and p65, concomitant with the increase in lipid deposition and inflammatory cytokine production. Together, these data indicate that miR-223 up-regulation might abrogate the development of atherosclerosis by blocking TLR4 signaling through activation of the PI3K/AKT pathway, and provides a promising therapeutic avenue for the treatment of 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.