ArticleProceedings of the National Academy of Sciences of the United States of America2015
Nuclear receptor RORα regulates pathologic retinal angiogenesis by modulating SOCS3-dependent inflammation.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
49 citing papers in PubMed, 68 citations in OpenAlex.
- Retinoic acid in health and disease.Signal transduction and targeted therapy · 2026Review
- Clock Modulation by Naringenin Suppresses Lipogenesis and Promotes Adipose Tissue Browning.Journal of cellular physiology · 2026Article
- Retinoic acid-related orphan receptor alpha (RORα) as a candidate multi-pathway target in Alzheimer's disease: mechanisms and therapeutic prospects.Frontiers in neuroscience · 2026Review
- Review
- Sleep Deprivation Activates a Conserved Lactate-H3K18la-RORα Axis Driving Neutrophilic Inflammation Across Species.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Sorting nexin 3 promotes ischemic retinopathy through RIP1- and RIP3-mediated myeloid cell necroptosis and mitochondrial fission.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Genetic Loss of RORα Impairs Visual Function With Rod Bipolar Cell Degeneration In Mice.Investigative ophthalmology & visual science · 2025Article
- Article
- Direct regulation of Per2 by Roraa: insights into circadian and metabolic interplay in zebrafish.Cellular and molecular life sciences : CMLS · 2025Article
- Transcriptomic and proteomic analyses of sclera in lens-induced myopic guinea pigs.BMC genomics · 2025Article
- SOCS3 regulates pathological retinal angiogenesis through modulating SPP1 expression in microglia and macrophages.Molecular therapy : the journal of the American Society of Gene Therapy · 2024Article
- FAM222A, Part of the BET-Regulated Basal Endothelial Transcriptome, Is a Novel Determinant of Endothelial Biology and Angiogenesis-Brief Report.Arteriosclerosis, thrombosis, and vascular biology · 2024Article
- Modulation of recovery from neonatal hyperoxic lung injury by sex as a biological variable.Redox biology · 2023Article
- Single-nucleus multiregion transcriptomic analysis of brain vasculature in Alzheimer's disease.Nature neuroscience · 2023Article
- Potential therapeutic targets for age-related macular degeneration: The nuclear option.Progress in retinal and eye research · 2023Review
- Effects of medications on hypoxia-inducible factor in the retina: A review.Clinical & experimental ophthalmology · 2023Review
- PGFEMBO molecular medicine · 2023Article
- Article
- Geographic atrophy: pathophysiology and current therapeutic strategies.Frontiers in ophthalmology · 2023Review
- Retinoic Acid Receptor-Related Orphan Receptors (RORs) in Eye Development and Disease.Advances in experimental medicine and biology · 2023Review
Corrections and comments
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Authors and funding
11 authors at 5 institutions in 2 countries.
Funding
Abstract
Pathologic ocular angiogenesis is a leading cause of blindness, influenced by both dysregulated lipid metabolism and inflammation. Retinoic-acid-receptor-related orphan receptor alpha (RORα) is a lipid-sensing nuclear receptor with diverse biologic function including regulation of lipid metabolism and inflammation; however, its role in pathologic retinal angiogenesis remains poorly understood. Using a mouse model of oxygen-induced proliferative retinopathy, we showed that RORα expression was significantly increased and genetic deficiency of RORα substantially suppressed pathologic retinal neovascularization. Loss of RORα led to decreased levels of proinflammatory cytokines and increased levels of antiinflammatory cytokines in retinopathy. RORα directly suppressed the gene transcription of suppressors of cytokine signaling 3 (SOCS3), a critical negative regulator of inflammation. Inhibition of SOCS3 abolished the antiinflammatory and vasoprotective effects of RORα deficiency in vitro and in vivo. Moreover, treatment with a RORα inverse agonist SR1001 effectively protected against pathologic neovascularization in both oxygen-induced retinopathy and another angiogenic model of very-low-density lipoprotein receptor (Vldlr)-deficient (Vldlr (-/-) ) mice with spontaneous subretinal neovascularization, whereas a RORα agonist worsened oxygen-induced retinopathy. Our data demonstrate that RORα is a novel regulator of pathologic retinal neovascularization, and RORα inhibition may represent a new way to treat ocular neovascularization.
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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.