ArticleProceedings of the National Academy of Sciences of the United States of America2020
An inhibitor of endothelial ETS transcription factors promotes physiologic and therapeutic vessel regression.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 29 citations in OpenAlex.
- TNFα and endothelial IL-1 receptor signaling drive peritubular capillary regression and mature collagen accumulation in obstructive kidney injury.American journal of physiology. Renal physiology · 2026Article
- EWSR1-SMAD3-rearranged fibroblastic tumor: a case report with literature review.Medical molecular morphology · 2026Article
- GPR124 regulates hyaloid blood vessel regression and is associated with endothelial-mesenchymal transition.Scientific reports · 2026Article
- TNFα and Endothelial IL-1 Receptor Signaling Drive Peritubular Capillary Regression and Fibrosis in Obstructive Kidney Injury.bioRxiv : the preprint server for biology · 2025Article
- Integrated Genomic-Metabolomic Analysis for Tri-Categorical Classification of Type 2 Diabetes Status in the Korean Ansan-Ansung Cohort.International journal of molecular sciences · 2025Article
- Epigenomic landscape of single vascular cells reflects developmental origin and disease risk loci.Molecular systems biology · 2025Article
- Targeting endothelial ERG to mitigate vascular regression in retinopathies.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- The epigenomic landscape of single vascular cells reflects developmental origin and identifies disease risk loci.bioRxiv : the preprint server for biology · 2025Article
- A targeted CRISPR screen identifies ETS1 as a regulator of HIV-1 latency.PLoS pathogens · 2025Article
- Role of Transcription Factor Fli-1 in Inflammation and Autoimmune Diseases.Biomolecules · 2025Review
- FLI-1-driven regulation of endothelial cells in human diseases.Journal of translational medicine · 2024Review
- EndothelialResearch square · 2024Article
- Stiffness-induced modulation of ERG transcription factor in chronic liver disease.Npj gut and liver · 2024Article
- Extracellular Matrix Remodeling in Vascular Disease: Defining Its Regulators and Pathological Influence.Arteriosclerosis, thrombosis, and vascular biology · 2023Review
- Identification and validation of lactate metabolism-related genes in oxygen-induced retinopathy.Scientific reports · 2023Article
- The roles of ETS transcription factors in liver fibrosis.Human cell · 2023Review
- Physiological and Pathological Remodeling of Cerebral Microvessels.International journal of molecular sciences · 2022Review
- Lymphatic Vessel Regression and Its Therapeutic Applications: Learning From Principles of Blood Vessel Regression.Frontiers in physiology · 2022Review
- Diabetic retinopathy: Involved cells, biomarkers, and treatments.Frontiers in pharmacology · 2022Review
- REST promotes ETS1-dependent vascular growth in medulloblastoma.Molecular oncology · 2021Article
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
Abstract
During the progression of ocular diseases such as retinopathy of prematurity and diabetic retinopathy, overgrowth of retinal blood vessels results in the formation of pathological neovascular tufts that impair vision. Current therapeutic options for treating these diseases include antiangiogenic strategies that can lead to the undesirable inhibition of normal vascular development. Therefore, strategies that eliminate pathological neovascular tufts while sparing normal blood vessels are needed. In this study we exploited the hyaloid vascular network in murine eyes, which naturally undergoes regression after birth, to gain mechanistic insights that could be therapeutically adapted for driving neovessel regression in ocular diseases. We found that endothelial cells of regressing hyaloid vessels underwent down-regulation of two structurally related E-26 transformation-specific (ETS) transcription factors, ETS-related gene (ERG) and Friend leukemia integration 1 (FLI1), prior to apoptosis. Moreover, the small molecule YK-4-279, which inhibits the transcriptional and biological activity of ETS factors, enhanced hyaloid regression in vivo and drove Human Umbilical Vein Endothelial Cells (HUVEC) tube regression and apoptosis in vitro. Importantly, exposure of HUVECs to sheer stress inhibited YK-4-279-induced apoptosis, indicating that low-flow vessels may be uniquely susceptible to YK-4-279-mediated regression. We tested this hypothesis by administering YK-4-279 to mice in an oxygen-induced retinopathy model that generates disorganized and poorly perfused neovascular tufts that mimic human ocular diseases. YK-4-279 treatment significantly reduced neovascular tufts while sparing healthy retinal vessels, thereby demonstrating the therapeutic potential of this inhibitor.
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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.