ArticlePloS one2014
Toll-like receptor 4 mediates inflammatory cytokine secretion in smooth muscle cells induced by oxidized low-density lipoprotein.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.
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Who cites it
46 citing papers in PubMed, 70 citations in OpenAlex.
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- Novel insights of ferroptosis in atherosclerosis progression.Frontiers in cell and developmental biology · 2026Review
- A Lipid Road to Neuroimmunology: Fatty Acids Linking Immune and Nervous Systems.Neuroimmunomodulation · 2026Review
- Decursin-Loaded Nanovesicles Target Macrophages Driven by the Pathological Process of Atherosclerosis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Inflammatory Pathways in Coronary Artery Disease: Which Ones to Target for Secondary Prevention?Cells · 2025Review
- Atherosclerosis and Toll-Like Receptor4 (TLR4), Lectin-Like Oxidized Low-Density Lipoprotein-1 (LOX-1), and Proprotein Convertase Subtilisin/Kexin Type9 (PCSK9).Mediators of inflammation · 2024Review
- Hif-1α/Slit2 Mediates Vascular Smooth Muscle Cell Phenotypic Changes in Restenosis of Bypass Grafts.Journal of cardiovascular translational research · 2023Article
- Article
- Investigation of TLR4 Antagonists for Prevention of Intestinal Inflammation.Inflammation · 2023Article
- Regulation by Nrf2 of IL-1β-induced inflammatory and oxidative response in VSMC and its relationship with TLR4.Frontiers in pharmacology · 2023Article
- TLR4 is one of the receptors for Chikungunya virus envelope protein E2 and regulates virus induced pro-inflammatory responses in host macrophages.Frontiers in immunology · 2023Article
- Regulation of gasdermins in pyroptosis and cytokine release.Advances in immunology · 2023Article
- Two-faced Janus: the dual role of macrophages in atherosclerotic calcification.Cardiovascular research · 2022Review
- Smooth muscle cell specific NEMO deficiency inhibits atherosclerosis in ApoEScientific reports · 2022Article
- Targeting Scavenger Receptors in Inflammatory Disorders and Oxidative Stress.Antioxidants (Basel, Switzerland) · 2022Review
- Glutathione: A Samsonian life-sustaining small molecule that protects against oxidative stress, ageing and damaging inflammation.Frontiers in nutrition · 2022Review
- Recent Progress of Chronic Stress in the Development of Atherosclerosis.Oxidative medicine and cellular longevity · 2022Review
- The interplay of DAMPs, TLR4, and proinflammatory cytokines in pulmonary fibrosis.Journal of molecular medicine (Berlin, Germany) · 2021Review
- Ultrasensitive Multiparameter Phenotyping of Rare Cells Using an Integrated Digital-Molecular-Counting Microfluidic Well Plate.Small (Weinheim an der Bergstrasse, Germany) · 2021Article
- Toll-Like Receptor 4 Mediated Oxidized Low-Density Lipoprotein-Induced Foam Cell Formation in Vascular Smooth Muscle Cells via Src and Sirt1/3 Pathway.Mediators of inflammation · 2021Article
Corrections and comments
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Oxidized low-density lipoprotein (oxLDL)-regulated secretion of inflammatory cytokines in smooth muscle cells (SMCs) is regarded as an important step in the progression of atherosclerosis; however, its underlying mechanism remains unclear. This study investigated the role of toll-like receptor 4 (TLR4) in oxLDL-induced expression of inflammatory cytokines in SMCs both in vivo and in vitro. We found that the levels of TLR4, interleukin 1-β (IL1-β), tumor necrosis factor-α (TNFα), monocyte chemoattractant protein 1 (MCP-1) and matrix metalloproteinase-2 (MMP-2) expression were increased in the SMCs of atherosclerotic plaques in patients with femoral artery stenosis. In cultured primary arterial SMCs from wild type mice, oxLDL caused dose- and time-dependent increase in the expression levels of TLR4 and cytokines. These effects were significantly weakened in arterial SMCs derived from TLR4 knockout mice (TLR4-/-). Moreover, the secretion of inflammatory cytokines was blocked by TLR4-specific antibodies in primary SMCs. Ox-LDL induced activation of p38 and NFκB was also inhibited in TLR4-/- primary SMCs or when treated with TLR4-specific antibodies. These results demonstrated that TLR4 is a crucial mediator in oxLDL-induced inflammatory cytokine expression and secretion, and p38 and NFκB activation.
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