ArticleInternational journal of oral science2024
Stromal thrombospondin 1 suppresses angiogenesis in oral submucous fibrosis.
Article in International journal of oral science, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 15 citations in OpenAlex.
- Fibrotic-Angiogenic Signaling Networks in Oral Submucous Fibrosis: Pathobiology and Therapeutic Targeting.International journal of molecular sciences · 2026Review
- IL-6 Promotes Pathological Angiogenesis in Oral Submucous Fibrosis by Suppressing USP10-VEGFR1 Interaction.Journal of cellular and molecular medicine · 2026Article
- Matricellular Proteins in Bladder Cancer: Context-Dependent Roles in Tumor Promotion and Suppression.International journal of molecular sciences · 2026Review
- THBS1: a biomarker for PCOS and its role in pathogenesis via the PI3K/AKT signaling pathway.Mammalian genome : official journal of the International Mammalian Genome Society · 2026Article
- Colony-stimulating factor-2 triggers NNMT-dependent myofibroblast activation in head and neck cancer.Oncogene · 2026Article
- Stem cell-driven biomedical technologies for tooth regeneration: engineering scaffolds, organoid models, and molecular targeted strategies.Stem cell research & therapy · 2026Review
- An organoid-guided roadmap for precision delivery of epigallocatechin gallate in oral submucous fibrosis.Frontiers in bioengineering and biotechnology · 2026Review
- Molecular mechanisms of therapeutic resistance in areca nut-associated oral squamous cell carcinoma: the interplay of chronic inflammation and epithelial-mesenchymal transition.Frontiers in oncology · 2026Review
- Biomaterial-based therapeutic strategies for oral submucous fibrosis.Frontiers in cell and developmental biology · 2026Review
- Heterogeneous mechanisms, risk stratification, and translational advances in the malignant transformation of oral potentially malignant disorders to oral squamous cell carcinoma.Frontiers in molecular biosciences · 2026Review
- Stem cell therapy targets THBS1 to reverse endometrial fibrosis.Frontiers in cell and developmental biology · 2026Article
- Attenuated crosstalk between urothelium and fibroblasts promotes ureteral stricture development.Frontiers in immunology · 2026Article
- The role of thrombospondin-1 in dermatological conditions.Frontiers in medicine · 2026Review
- Distinctive tumor biology of oral squamous cell carcinoma associated with oral submucous fibrosis and its suppressive immune microenvironment.BMC oral health · 2025Article
- Review
- Abnormal collagen deposition mediated by cartilage oligomeric matrix protein in the pathogenesis of oral submucous fibrosis.International journal of oral science · 2025Article
- Oral submucous fibrosis: pathogenesis and therapeutic approaches.International journal of oral science · 2025Review
- THBS1 as a candidate biomarker and fibrotic mediator in radiation-induced liver injury: insights from TMT-labeled quantitative proteomics.Frontiers in pharmacology · 2025Article
- Organoids in the oral and maxillofacial region: present and future.International journal of oral science · 2024Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
A decline in mucosal vascularity is a histological hallmark of oral submucous fibrosis (OSF), a premalignant disease that is largely induced by betel quid chewing. However, the lack of available models has challenged studies of angiogenesis in OSF. Here, we found that the expression of thrombospondin 1 (THBS1), an endogenous angiostatic protein, was elevated in the stroma of tissues with OSF. Using a fibroblast-attached organoid (FAO) model, the overexpression of THBS1 in OSF was stably recapitulated in vitro. In the FAO model, treatment with arecoline, a major pathogenic component in areca nuts, enhanced the secretion of transforming growth factor (TGF)-β1 by epithelial cells, which then promoted the expression of THBS1 in fibroblasts. Furthermore, human umbilical vein endothelial cells (HUVECs) were incorporated into the FAO to mimic the vascularized component. Overexpression of THBS1 in fibroblasts drastically suppressed the sprouting ability of endothelial cells in vascularized FAOs (vFAOs). Consistently, treatment with arecoline reduced the expression of CD31 in vFAOs, and this effect was attenuated when the endothelial cells were preincubated with neutralizing antibody of CD36, a receptor of THBS1. Finally, in an arecoline-induced rat OSF model, THBS1 inhibition alleviated collagen deposition and the decline in vascularity in vivo. Overall, we exploited an assembled organoid model to study OSF pathogenesis and provide a rationale for targeting THBS1.
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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.