ArticleJACC. Basic to translational science2024
Endothelial Overexpression of TGF-β-Induced Protein Impairs Venous Thrombus Resolution: Possible Role in CTEPH.
Article in JACC. Basic to translational science, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 20 citations in OpenAlex.
- Potential association of TGFβ1 plasma levels and fibrinolysis parameters with the risk of recurrence and vascular obstruction after a first unprovoked pulmonary embolism episode.Journal of thrombosis and thrombolysis · 2025Trial
- Single-cell transcriptomics reveals NDRG1/TGF‑β1 associated vascular smooth muscle cell phenotypic switching in chronic thromboembolic pulmonary hypertension.Journal of thrombosis and thrombolysis · 2026Article
- Visualization of new vessel formation during venous thrombus organization using genetic fate mapping.Research and practice in thrombosis and haemostasis · 2026Article
- The MCP-1/CCR2-CD16⁺ monocyte axis drives thrombus fibrosis in Chronic Thromboembolic Pulmonary Hypertension.Journal of translational medicine · 2026Article
- TGF-β-induced autophagy in pulmonary artery endothelial cells associated with chronic thromboembolic pulmonary hypertension.Journal of molecular medicine (Berlin, Germany) · 2026Article
- Novel Plasma Proteomic Markers and Risk of Venous Thromboembolism.Circulation · 2026Article
- TGFBI promotes liver fibrosis through remodeling the profibrotic microenvironment by a positive feedback regulatory loop.Communications biology · 2026Article
- Research advances in chronic thromboembolic pulmonary hypertension: from pathological mechanisms to multidisciplinary management.Frontiers in cardiovascular medicine · 2026Review
- Transmembrane Protein 100 Expression on Endothelial Cells Vascularizing Thrombi in Chronic Thromboembolic Pulmonary Hypertension Modulates TGFβ1-ALK1 Signaling During Angiogenesis.Pulmonary circulation · 2026Article
- Notch signaling enhances PASMC proliferation and vascular remodeling in CTEPH.Open life sciences · 2026Article
- BIGH3 as a potential biomarker for fibrosis in metabolic dysfunction-associated steatotic liver disease: insights from mouse and human studies.BMC gastroenterology · 2025Article
- Regulation of inflammatory lung injury and repair by transforming growth factors.American journal of physiology. Lung cellular and molecular physiology · 2025Review
- The activin pathway in chronic thromboembolic pulmonary hypertension: a potential biomarker for residual pulmonary hypertension after endarterectomy.ERJ open research · 2025Article
- Distinct endothelial cells in chronic thromboembolic pulmonary hypertension.NPJ cardiovascular health · 2025Article
- Transforming Growth Factors in Venous Thrombus Formation and Resolution.Arteriosclerosis, thrombosis, and vascular biology · 2025Review
- Endothelial Features Along the Pulmonary Vascular Tree in Chronic Thromboembolic Pulmonary Hypertension: Distinctive or Shared Facets?Pulmonary circulation · 2025Article
- SPHK1-mediated M2 macrophage polarization drives TGF-β1-dependent thrombus fibrosis.Frontiers in immunology · 2025Article
- Revealing the impact ofFrontiers in immunology · 2025Article
- Molecular Pathophysiology of Chronic Thromboembolic Pulmonary Hypertension: A Clinical Update from a Basic Research Perspective.Advances in respiratory medicine · 2024Review
- Expression ofGenes · 2024Article
Corrections and comments
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Authors and funding
13 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Endothelial cells play a critical role during venous thrombus remodeling, and unresolved, fibrotic thrombi with irregular vessels obstruct the pulmonary artery in patients with chronic thromboembolic pulmonary hypertension (CTEPH). This study sought to identify endothelial mediators of impaired venous thrombus resolution and to determine their role in the pathogenesis of the vascular obstructions in patients with CTEPH. Endothelial cells outgrown from pulmonary endarterectomy specimens (PEA) were processed for mRNA profiling, and nCounter gene expression and immunohistochemistry analysis of PEA tissue microarrays and immunoassays of plasma were used to validate the expression in CTEPH. Lentiviral overexpression in human pulmonary artery endothelial cells (HPAECs) and exogenous administration of the recombinant protein into C57BL/6J mice after inferior Vena cava ligation were employed to assess their role for venous thrombus resolution. RT2 PCR profiler analysis demonstrated the significant overexpression of factors downstream of transforming growth factor beta (TGFβ), that is TGFβ-Induced Protein (TGFBI or BIGH3) and transgelin (TAGLN), or involved in TGFβ signaling, that is follistatin-like 3 (FSTL3) and stanniocalcin-2 (STC2). Gene expression and immunohistochemistry analysis of tissue microarrays localized potential disease candidates to vessel-rich regions. Lentiviral overexpression of TGFBI in HPAECs increased fibrotic remodeling of human blood clots in vitro, and exogenous administration of recombinant TGFBI in mice delayed venous thrombus resolution. Significantly elevated plasma TGFBI levels were observed in patients with CTEPH and decreased after PEA. Our findings suggest that overexpression of TGFBI in endothelial promotes venous thrombus non-resolution and fibrosis and is causally involved in the pathophysiology of CTEPH.
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