ReviewSeminars in cell & developmental biology2022
Tenascin-C in fibrosis in multiple organs: Translational implications.
Review in Seminars in cell & developmental biology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 51 citations in OpenAlex.
- POSTN(+) fibroblasts and SPP1(+) macrophages in scar formation: A review of mechanisms and therapeutic targets (Review).Molecular medicine reports · 2026Review
- DAMP signaling networks: from receptors to diverse pathophysiological functions.Journal of advanced research · 2026Review
- Spatially controlled tenascin-C accumulation contributes to inflammatory disease persistence in giant cell aortitis.JCI insight · 2026Article
- Tissue-layer-resolved proteome landscape of Crohn's disease strictures highlights potential drivers of fibrosis progression.JCI insight · 2026Article
- Single cell RNA-seq characterization of non-fibrotic stromal wound repopulation in the rabbit.Experimental eye research · 2026Article
- Combined antagonism of Oncostatin M (OSM) and Interleukin 6 (IL-6) provides both anti-fibrotic and anti-inflammatory benefit in pulmonary fibrosis.bioRxiv : the preprint server for biology · 2026Article
- Tenascin-C from the tissue microenvironment promotes muscle stem cell maintenance and function through Annexin A2.Communications biology · 2025Article
- TNC-targeted CAR-macrophage therapy alleviates liver fibrosis in mice.Military Medical Research · 2025Article
- The Role of Tenascin-C in Neuroinflammation and Neuroplasticity.International journal of molecular sciences · 2025Review
- Deconstruction of cellular dynamics after treatment of volumetric muscle loss injury with extracellular matrix.NPJ Regenerative medicine · 2025Article
- Cold, Hot, and Lethal-The Tumour Microenvironment and the Immunology of Head and Neck Squamous Cell Carcinoma.International journal of molecular sciences · 2025Review
- Deciphering the Tenascin-C Nexus: A Comprehensive Review of Its Involvement in Chronic Respiratory Diseases.Pathophysiology : the official journal of the International Society for Pathophysiology · 2025Review
- METTL3-mediated m⁶A methylation in cardiac diseases: pathogenic roles and therapeutic potential.Cell biology and toxicology · 2025Review
- Paw Skin as a Translational Model for Investigating Fibrotic and Inflammatory Wound Healing Defects in Recessive Dystrophic Epidermolysis Bullosa.International journal of molecular sciences · 2025Article
- Direct fibroblast reprogramming: an emerging strategy for treating organic fibrosis.Journal of translational medicine · 2025Review
- SPP1hi macrophages, NKG7 T cells, CCL5hi fibroblasts, and IgM plasma cells are dominant features of necrobiosis.JCI insight · 2025Article
- Profiling of Toll-like Receptors and Related Signaling Mediators in the Pathogenesis of Morphea.Dermatology practical & conceptual · 2024Article
- Identification of a fibronectin-binding protein signature associated with idiopathic pulmonary fibrosis.Cells & development · 2024Article
- Engineered Microenvironmental Cues from Fiber-Reinforced Hydrogel Composites Drive Tenogenesis and Aligned Collagen Deposition.Advanced healthcare materials · 2024Article
- Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Systemic sclerosis (SSc, scleroderma) is a complex disease with a pathogenic triad of autoimmunity, vasculopathy, and fibrosis involving the skin and multiple internal organs [1]. Because fibrosis accounts for as much as 45% of all deaths worldwide and appears to be increasing in prevalence [2], understanding its pathogenesis and progression is an urgent scientific challenge. Fibroblasts and myofibroblasts are the key effector cells executing physiologic tissue repair on one hand, and pathological fibrogenesis leading to chronic fibrosing conditions on the other. Recent studies identify innate immune signaling via toll-like receptors (TLRs) as a key driver of persistent fibrotic response in SSc. Repeated injury triggers the in-situ generation of "damage-associated molecular patterns" (DAMPs) or danger signals. Sensing of these danger signals by TLR4 on resident cells elicits potent stimulatory effects on fibrotic gene expression and myofibroblast differentiation triggering the self-limited tissue repair response to self-sustained pathological fibrosis characteristic of SSc. Our unbiased survey for DAMPs associated with SSc identified extracellular matrix glycoprotein tenascin-C as one of the most highly up-regulated ECM proteins in SSc skin and lung biopsies [3,4]. Furthermore, tenascin C is responsible for driving sustained fibroblasts activation, thereby progression of fibrosis [3]. This review summarizes recent studies examining the regulation and complex functional role of tenascin C, presenting tenascin-TLR4 axis in pathological fibrosis, and novel anti-fibrotic approaches targeting their signaling.
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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.