ArticleNature communications2017
Mapping tenascin-C interaction with toll-like receptor 4 reveals a new subset of endogenous inflammatory triggers.
Article in Nature communications, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 80 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.
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Who cites it
80 citing papers in PubMed, 112 citations in OpenAlex.
- Biochemical signals from the extracellular matrix in inflammation and tumour immunology.Nature reviews. Immunology · 2026Review
- The impact of inflammation, neuromodulation, and gut microbiota on developing cardiac fibrosis and hypertension.Cardiovascular research · 2026Review
- Single nuclei/cell transcriptomics reveal DMD driven cell dynamics and mechanisms of fibroblast inflammatory tissue priming in human dystrophic muscle.Research square · 2026Article
- Piezo1-dependent activation of stromal cells ignites muscle inflammation in exercise and injury and is associated with inflammaging.Nature immunology · 2026Article
- Article
- Host TLR4 activation by tenascin-C is associated with MMP14-dependent glioma invasion.Frontiers in oncology · 2026Article
- Article
- Increased TNN in Knee Osteoarthritis Accelerates Cartilage Damage via the Negative Regulation of AMPK-PPARγ Signalling.Journal of cellular and molecular medicine · 2025Article
- The Role of Tenascin-C in Neuroinflammation and Neuroplasticity.International journal of molecular sciences · 2025Review
- Sustained tenascin-C expression drives neointimal hyperplasia and promotes aortocaval fistula failure.American journal of physiology. Heart and circulatory physiology · 2025Article
- Tenascin-C drives cardiovascular dysfunction in a mouse model of diabetic cardiomyopathy.Cardiovascular diabetology · 2025Article
- Necrosis-like cell death modes in heart failure: the influence of aetiology and the effects of RIP3 inhibition.Basic research in cardiology · 2025Article
- The Marine Compound Isaridin E Ameliorates Lipopolysaccharide-Induced Vascular Endothelial Inflammation via the Downregulation of the TLR4/NF-κB Signaling Pathway.Marine drugs · 2025Article
- Tau Pathology Drives Disease-Associated Astrocyte Reactivity in Salt-Induced Neurodegeneration.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Negative regulation of lymphangiogenesis by Tenascin-C delays the resolution of inflammation.iScience · 2025Article
- Development of a 3D tumor model based on decellularized matrix using high-throughput approaches.Frontiers in bioengineering and biotechnology · 2025Review
- An Improved RNA Extraction Method for Octocorals and Its Application in Transcriptome Analysis of Dark-Induced Bleaching Octocoral.Marine biotechnology (New York, N.Y.) · 2024Article
- Distinct tumor architectures and microenvironments for the initiation of breast cancer metastasis in the brain.Cancer cell · 2024Article
- The evolution of tenascins.BMC ecology and evolution · 2024Article
- Inflammasomes as regulators of mechano-immunity.EMBO reports · 2024Review
20 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
Pattern recognition underpins innate immunity; the accurate identification of danger, including infection, injury, or tumor, is key to an appropriately targeted immune response. Pathogen detection is increasingly well defined mechanistically, but the discrimination of endogenous inflammatory triggers remains unclear. Tenascin-C, a matrix protein induced upon tissue damage and expressed by tumors, activates toll-like receptor 4 (TLR4)-mediated sterile inflammation. Here we map three sites within tenascin-C that directly and cooperatively interact with TLR4. We also identify a conserved inflammatory epitope in related proteins from diverse families, and demonstrate that its presence targets molecules for TLR detection, while its absence enables escape of innate immune surveillance. These data reveal a unique molecular code that defines endogenous proteins as inflammatory stimuli by marking them for recognition by TLRs.
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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.