ArticleAmerican journal of respiratory cell and molecular biology2025
SOX17 Prevents Endothelial-Mesenchymal Transition of Pulmonary Arterial Endothelial Cells in Pulmonary Hypertension through Mediating TGF-β/Smad2/3 Signaling.
Article in American journal of respiratory cell and molecular biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Precision nanomedicine for pulmonary diseases: from molecular targeting to clinical translation.Signal transduction and targeted therapy · 2026Review
- Identification of drug candidates for rescue of SOX17 gene targets in pulmonary arterial hypertension.bioRxiv : the preprint server for biology · 2026Article
- Altitude hypoxia and hypoxemia: pathogenesis and management.Signal transduction and targeted therapy · 2026Review
- Current Evidence on the Potential Role of EndothelialReviews in cardiovascular medicine · 2026Review
- SOX17 in pulmonary arterial hypertension: from development to clinical phenotype.European respiratory review : an official journal of the European Respiratory Society · 2025Review
- Guarding the Endothelium: SOX17's Crucial Role in Pulmonary Hypertension.American journal of respiratory cell and molecular biology · 2025Article
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Funding
Abstract
Endothelial-to-mesenchymal transition (EndMT) has been reported to contribute to pulmonary vascular remodeling in patients with pulmonary hypertension (PH). Our study demonstrates that SOX17, a member of the SOX (SRY-Box) transcription factor family, plays a role in regulating pulmonary arterial homeostasis through extracellular vesicles in an autocrine and paracrine manner. However, the role of SOX17 in mediating EndMT of pulmonary arterial endothelial cells (PAECs) and its intracellular mechanisms remain unclear. Here we present evidence showing that downregulation of SOX17 expression is accompanied by significant pulmonary arterial EndMT and activation of the TGF-β/Smad2/3 signaling pathway in patients with idiopathic PH and rats with PH induced by Sugen 5416/hypoxia. In primary human PAECs, canonical TGF-β (transforming growth factor-β) signaling inhibits the expression of SOX17. Overexpression of SOX17 reverses TGF-β- and hypoxia-induced EndMT. These findings suggest that SOX17 is essential for human PAECs to undergo TGF-β-mediated EndMT. Mechanistically, our data demonstrate that SOX17 prevents TGF-β-induced EndMT by suppressing ROCK1 (Rho-associated kinase 1) expression through binding to the specific promoter region of ROCK1, thereby inhibiting MYPT1 (myosin phosphatase target subunit 1) and MLC (myosin light chain) phosphorylation. Furthermore, we show that Tie2-Cre rats with endothelial cell-specific overexpression of SOX17 are protected against Sugen/hypoxia-induced EndMT and subsequent pulmonary vascular remodeling. Consistent with the
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