ArticleMolecules and cells2012
Tenascin-C produced by oxidized LDL-stimulated macrophages increases foam cell formation through Toll-like receptor-4.
Article in Molecules and cells, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
17 citing papers in PubMed, 31 citations in OpenAlex.
- Identification and validation of efferocytosis-related biomarkers for the diagnosis of atherosclerosis based on bioinformatics and machine learning.European journal of medical research · 2025Article
- Role of Matricellular Proteins in Endothelial Cell Inflammation and Atherosclerosis.Antioxidants (Basel, Switzerland) · 2025Review
- Tenascin-C and Thrombospondin-1 as a Potential Link Between Sleep Bruxism and Cardiovascular Diseases-A Case-Control Study.Journal of clinical medicine · 2025Article
- Bioactive TNIIIA2 Sequence in Tenascin-C Is Responsible for Macrophage Foam Cell Transformation; Potential of FNIII14 Peptide Derived from Fibronectin in Suppression of Atherosclerotic Plaque Formation.International journal of molecular sciences · 2024Article
- The role of TNC in atherosclerosis and drug development opportunities.International journal of biological sciences · 2024Review
- Matricellular proteins in atherosclerosis development.Matrix biology : journal of the International Society for Matrix Biology · 2023Review
- Advances on the roles of tenascin-C in cancer.Journal of cell science · 2022Article
- Identification of molecular subtypes of coronary artery disease based on ferroptosis- and necroptosis-related genes.Frontiers in genetics · 2022Article
- Extracellular Vesicles: An Emerging Mechanism Governing the Secretion and Biological Roles of Tenascin-C.Frontiers in immunology · 2021Review
- The Roles of Tenascins in Cardiovascular, Inflammatory, and Heritable Connective Tissue Diseases.Frontiers in immunology · 2020Review
- Transcriptome Profiling of Bovine Macrophages Infected byFrontiers in immunology · 2019Article
- Internal Affairs: Tenascin-C as a Clinically Relevant, Endogenous Driver of Innate Immunity.The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2018Review
- Tenascin-C drives persistence of organ fibrosis.Nature communications · 2016Article
- Toll-like Receptors in the Vascular System: Sensing the Dangers Within.Pharmacological reviews · 2016Review
- Extracellular matrix regulation of inflammation in the healthy and injured spinal cord.Experimental neurology · 2014Review
- miR-21 attenuates lipopolysaccharide-induced lipid accumulation and inflammatory response: potential role in cerebrovascular disease.Lipids in health and disease · 2014Article
- Damage-associated molecular patterns and their receptors in upper airway pathologies.Cellular and molecular life sciences : CMLS · 2013Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Atherosclerosis is a chronic inflammatory disease in which both innate and adaptive immunity are involved. Although there have been major advances in the involvement of toll-like receptor 4 (TLR4) and CD36 in the initiation and development of this disease, detailed mechanisms remain unknown. Here, we show that tenascin-C (TN-C) can stimulate foam cell formation and this can be inhibited by a TLR4-blocking antibody or CD36 gene silencing. Our results identify TN-C-TLR4 activation as a common molecular mechanism in oxLDL-stimulated foam cell formation and atherosclerosis. In addition, CD36 is the major scavenger receptor responsible for the TN-C-mediated foam cell formation. Taken together, we have identified that TNC produced by oxLDL-stimulated macrophages increases foam cell formation through TLR4 and scavenger receptor CD36.
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What OpenQuestion holds
Registered trials
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.