ArticleJCI insight2021
Role of endothelial cells in pulmonary fibrosis via SREBP2 activation.
Article in JCI insight, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 44 citations in OpenAlex.
- LATS1/2 inactivation drives a distinct venous endothelial cell response that contributes to fibrotic remodeling of the lung.Science advances · 2026Article
- EndMT in vascular cognitive impairment and dementia: mechanisms, evidence gaps, and therapeutic opportunities.Molecular medicine (Cambridge, Mass.) · 2026Review
- From Heterogeneity to Plasticity: Endothelial Dynamics in Lung Disease.Pulmonary circulation · 2026Review
- Network medicine modeling of the m⁶A regulatory landscape identifies a KLF6-WTAP axis as a therapeutic target in pulmonary fibrosis.Journal of translational medicine · 2026Article
- Treadmill exercise activates mechanosensitive Piezo1 to inhibit cardiomyocyte apoptosis and improve cardiac function after myocardial infarction in mice.Basic research in cardiology · 2026Article
- Pulmonary Fibrosis-Focusing on the Future: Aspen Lung Conference 2024 Summary.American journal of respiratory cell and molecular biology · 2025Article
- Vascular protection by young circulating extracellular vesicles ameliorates aging-related pulmonary fibrosis.American journal of physiology. Cell physiology · 2025Article
- New perspectives on the progression of pulmonary fibrosis: the cascade from aberrant microvascular endothelial cell activation to fibrosis.Frontiers in medicine · 2025Review
- The role of epithelial-mesenchymal transition in pulmonary fibrosis: lessons from idiopathic pulmonary fibrosis and COVID-19.Cell communication and signaling : CCS · 2024Review
- Ailanthone ameliorates pulmonary fibrosis by suppressing JUN-dependent MEOX1 activation.Acta pharmaceutica Sinica. B · 2024Article
- The novel molecular mechanism of pulmonary fibrosis: insight into lipid metabolism from reanalysis of single-cell RNA-seq databases.Lipids in health and disease · 2024Review
- Cancer‑associated fibroblasts under therapy‑induced senescence in the tumor microenvironment (Review).Experimental and therapeutic medicine · 2024Review
- Necroptosis inhibitors: mechanisms of action and therapeutic potential.Apoptosis : an international journal on programmed cell death · 2024Review
- MicroRNA‑203a‑3p improves bleomycin and pingyangmycin sensitivity by inactivating the PI3K/AKT pathway in hemangioma.Experimental and therapeutic medicine · 2024Article
- Biogenesis and Function of circRNAs in Pulmonary Fibrosis.Current gene therapy · 2024Review
- Identification of the novel role of sterol regulatory element binding proteins (SREBPs) in mechanotransduction and intraocular pressure regulation.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2023Article
- Beyond epithelial damage: vascular and endothelial contributions to idiopathic pulmonary fibrosis.The Journal of clinical investigation · 2023Review
- The vascular perspective on acute and chronic lung disease.The Journal of clinical investigation · 2023Review
- Vascular Contribution to Lung Repair and Fibrosis.American journal of respiratory cell and molecular biology · 2023Review
- Injured Endothelial Cell: A Risk Factor for Pulmonary Fibrosis.International journal of molecular sciences · 2023Review
Corrections and comments
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Authors and funding
20 authors at 6 institutions in 3 countries.
Funding
Abstract
Idiopathic pulmonary fibrosis (IPF) is a progressive lung disease with limited treatment options. Despite endothelial cells (ECs) comprising 30% of the lung cellular composition, the role of EC dysfunction in pulmonary fibrosis (PF) remains unclear. We hypothesize that sterol regulatory element-binding protein 2 (SREBP2) plays a critical role in the pathogenesis of PF via EC phenotypic modifications. Transcriptome data demonstrate that SREBP2 overexpression in ECs led to the induction of the TGF, Wnt, and cytoskeleton remodeling gene ontology pathways and the increased expression of mesenchymal genes, such as snail family transcriptional repressor 1 (snai1), α-smooth muscle actin, vimentin, and neural cadherin. Furthermore, SREBP2 directly bound to the promoter regions and transactivated these mesenchymal genes. This transcriptomic change was associated with an epigenetic and phenotypic switch in ECs, leading to increased proliferation, stress fiber formation, and ECM deposition. Mice with endothelial-specific transgenic overexpression of SREBP2 (EC-SREBP2[N]-Tg mice) that were administered bleomycin to induce PF demonstrated exacerbated vascular remodeling and increased mesenchymal transition in the lung. SREBP2 was also found to be markedly increased in lung specimens from patients with IPF. These results suggest that SREBP2, induced by lung injury, can exacerbate PF in rodent models and in human patients with IPF.
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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.