ArticleThe American journal of pathology2012
MEF2C ablation in endothelial cells reduces retinal vessel loss and suppresses pathologic retinal neovascularization in oxygen-induced retinopathy.
Article in The American journal of pathology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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Who cites it
41 citing papers in PubMed, 70 citations in OpenAlex.
- A MEF2C transcription factor network regulates proliferation of glomerular endothelial cells in diabetic kidney disease.Kidney international · 2026Article
- Alternative splicing and polyadenylation facilitate transcriptome diversity underlying high-altitude adaptation in pigs.Communications biology · 2026Article
- The Role of MEF2 in Scar Formation and Angiogenesis.Journal of cosmetic dermatology · 2026Review
- Atypical p38 Kinase Signaling in Retinal Vascular Damage and Recovery.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- Spatial transcriptomics reveals regionally altered gene expression that drives retinal degeneration.Communications biology · 2025Article
- Mef2c Exacerbates Neuron Necroptosis via Modulating Alternative Splicing of Cflar in Ischemic Stroke With Hyperlipidemia.CNS neuroscience & therapeutics · 2024Article
- Transcription factors regulating vasculogenesis and angiogenesis.Developmental dynamics : an official publication of the American Association of Anatomists · 2024Review
- Role of MEF2C in the Endothelial Cells Derived from Human Induced Pluripotent Stem Cells.Stem cells (Dayton, Ohio) · 2023Article
- CD36Cell discovery · 2023Article
- Role of acyl-coenzyme A: cholesterol transferase 1 (ACAT1) in retinal neovascularization.Journal of neuroinflammation · 2023Article
- Myeloid cell modulation by a GLP-1 receptor agonist regulates retinal angiogenesis in ischemic retinopathy.JCI insight · 2021Article
- Coming of Age for the Photoreceptor Synapse.Investigative ophthalmology & visual science · 2021Article
- MEF2 (Myocyte Enhancer Factor 2) Is Essential for Endothelial Homeostasis and the Atheroprotective Gene Expression Program.Arteriosclerosis, thrombosis, and vascular biology · 2021Article
- Article
- The Role of Apelin/APJ in a Mouse Model of Oxygen-induced Retinopathy.Investigative ophthalmology & visual science · 2020Article
- Vascular and Neuronal Protection in the Developing Retina: Potential Therapeutic Targets for Retinopathy of Prematurity.International journal of molecular sciences · 2019Review
- Cardiovascular development and survival require Mef2c function in the myocardial but not the endothelial lineage.Developmental biology · 2019Article
- Morphology regulation in vascular endothelial cells.Inflammation and regeneration · 2018Review
- Exosomal MicroRNA-15a Transfer from the Pancreas Augments Diabetic Complications by Inducing Oxidative Stress.Antioxidants & redox signaling · 2017Article
- MiR-448 promotes vascular smooth muscle cell proliferation and migration in through directly targeting MEF2C.Environmental science and pollution research international · 2017Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
Abstract
Ischemic retinopathies, including retinopathy of prematurity and diabetic retinopathy, are major causes of blindness. Both have two phases, vessel loss and consequent hypoxia-driven pathologic retinal neovascularization, yet relatively little is known about the transcription factors regulating these processes. Myocyte enhancer factor 2 (MEF2) C, a member of the MEF2 family of transcription factors that plays an important role in multiple developmental programs, including the cardiovascular system, seems to have a significant functional role in the vasculature. We, therefore, generated endothelial cell (EC)-specific MEF2C-deficient mice and explored the role of MEF2C in retinal vascularization during normal development and in a mouse model of oxygen-induced retinopathy. Ablation of MEF2C did not cause appreciable defects in normal retinal vascular development. However, MEF2C ablation in ECs suppressed vessel loss in oxygen-induced retinopathy and strongly promoted vascular regrowth, consequently reducing retinal avascularity. This finding was associated with suppression of pathologic retinal angiogenesis and blood-retinal barrier dysfunction. MEF2C knockdown in cultured retinal ECs using small-interfering RNAs rescued ECs from death and stimulated tube formation under stress conditions, confirming the endothelial-autonomous and antiangiogenic roles of MEF2C. HO-1 was induced by MEF2C knockdown in vitro and may play a role in the proangiogenic effect of MEF2C knockdown on retinal EC tube formation. Thus, MEF2C may play an antiangiogenic role in retinal ECs under stress conditions, and modulation of MEF2C may prevent pathologic retinal 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.