ArticleAtherosclerosis2016
Tumor necrosis factor-α regulates triggering receptor expressed on myeloid cells-1-dependent matrix metalloproteinases in the carotid plaques of symptomatic patients with carotid stenosis.
Article in Atherosclerosis, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.
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Who cites it
48 citing papers in PubMed, 64 citations in OpenAlex.
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- Triggering receptor expressed on myeloid cell family in atherosclerosis: from mechanisms to intervention strategies.Cell communication and signaling : CCS · 2026Review
- Identification of key genes and signaling pathways associated with acute pancreatitis and acute lung injury by bioinformatics analysis.PloS one · 2026Article
- The Multifaceted Role of Platelets in Atherosclerosis and Ischemic Disease: Pathogenesis, Inflammation, and Therapeutic Opportunities.Life (Basel, Switzerland) · 2025Review
- Review
- The Exacerbating Effects of the Tumor Necrosis Factor in Cardiovascular Stenosis: Intimal Hyperplasia.Cancers · 2024Review
- Role of sirtuins in attenuating plaque vulnerability in atherosclerosis.Molecular and cellular biochemistry · 2024Review
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- Qili Qiangxin capsule attenuates myocardial fibrosis by modulating collagen homeostasis post-infarction in rats.PloS one · 2024Article
- Targeting Oncostatin M Receptor to Attenuate Carotid Artery Plaque Vulnerability in Hypercholesterolemic Microswine.Cardiology and cardiovascular medicine · 2024Article
- Therapeutic Potential of Targeting p27Archives of internal medicine research · 2024Article
- Increased Oxidative Stress and Decreased Sirtuin-3 and FOXO3 Expression Following Carotid Artery Intimal Injury in Hyperlipidemic Yucatan Microswine.Cardiology and cardiovascular medicine · 2024Article
- Residual risks and evolving atherosclerotic plaques.Molecular and cellular biochemistry · 2023Review
- Role of oncostatin-M in ECM remodeling and plaque vulnerability.Molecular and cellular biochemistry · 2023Review
- Oxidized Low-density Lipoproteins and Lipopolysaccharides Augment Carotid Artery Plaque Vulnerability in Hypercholesterolemic Microswine.Cardiology and cardiovascular medicine · 2023Article
- Regulation of Collagen I and Collagen III in Tissue Injury and Regeneration.Cardiology and cardiovascular medicine · 2023Article
- Similar collagen distribution in full-thickness skin grafts in intraperitoneal and onlay positions, an experimental mice-study.Hernia : the journal of hernias and abdominal wall surgery · 2022Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
objectiveTo determine the relationship between increased triggering receptor expressed on myeloid cells (TREM)-1 and plaque stability in atherosclerotic carotid stenosis.
methodsThe mRNA transcripts and protein for TREM-1, MMP-1, MMP-9, collagen type I (COL1A1) and collagen type III (COL3A1) were analyzed by qPCR and immunofluorescence in both tissues and VSMCs isolated from atherosclerotic carotid plaques of symptomatic and asymptomatic patients with carotid stenosis.
resultsThe TREM-1, MMP-1 and MMP-9 mRNA transcripts were significantly increased (TREM-1, p < 0.01; MMP-1, p < 0.01 and MMP-9, p < 0.001) while COL1A1 and COL3A1 mRNA transcripts were decreased (p < 0.001) in VSMCs isolated from carotid plaques of symptomatic (S) than asymptomatic (AS) patients. Stimulation of cells with TNF-α further increased the mRNA transcripts of TREM-1, MMPs, COL1A1 and COL3A1. Modulation of TREM-1 by treatment with TREM-1 decoy receptor rTREM-1/Fc, and either TREM-1 antibodies or TREM-1 siRNA attenuated the TNF-α-induced expression of MMP-1 and MMP-9 (p < 0.01) and COL1A1 and COL3A1 (p < 0.01) in S compared to AS VSMCs isolated from carotid plaques. Inhibition of NF-kB (BAY 11-7085), JNK (SP600125) and PI3K (LY294002) signaling pathways decreased the expression of TREM-1 (p < 0.01), MMP-1 (p < 0.001) and MMP-9 (p < 0.01) in TNF-α-treated VSMCs isolated from S carotid plaques compared to AS patients.
conclusionIncreased expression of TREM-1 in S compared to AS patients involving MMP-1 and MMP-9 suggest a potential role of TREM-1 in plaque destabilization. Selective blockade of TREM-1 may contribute to the development of new therapies and promising targets for stabilizing vulnerable atherosclerotic plaques.
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Registered trials
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