ArticleThe Journal of clinical investigation2021
Endothelium-derived semaphorin 3G attenuates ischemic retinopathy by coordinating β-catenin-dependent vascular remodeling.
Article in The Journal of clinical investigation, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed, 69 citations in OpenAlex.
- Semaphorin 3G (SEMA3G) is a highly selective marker of cerebral amyloid angiopathy.bioRxiv : the preprint server for biology · 2026Article
- FBXW7 mitigates hepatic fibrosis by degrading NOTCH1 to transcriptionally silence SEMA3G in liver sinusoidal endothelial cells.Nature communications · 2026Article
- Blood and lymphatic vascular network in bone injury repair: from molecular mechanisms to therapeutic strategies.Science China. Life sciences · 2026Review
- Neuron-Derived Sema3B Facilitates Microglial Hematoma Clearance After Intracerebral Hemorrhage.Antioxidants (Basel, Switzerland) · 2026Article
- Methyltransferase-like 14 suppresses the retinal neovascularization by reducing HIF-1α in proliferative retinopathy.European journal of medical research · 2026Article
- Endothelial cells-derived SEMA3G suppresses glioblastoma stem cells by inducing c-Myc degradation.Cell death and differentiation · 2025Article
- Immunomodulation of inflammatory responses preserves retinal integrity in murine models of pericyte-depletion retinopathy.JCI insight · 2025Article
- Pioneer factor ETV2 safeguards endothelial cell specification by recruiting the repressor REST to restrict alternative lineage commitment.Nature cardiovascular research · 2025Article
- SCIG: Machine learning uncovers cell identity genes in single cells by genetic sequence codes.Nucleic acids research · 2025Article
- β-Hydroxybutyrate Facilitates Homeostasis of Hypoxic Endothelial Cells After Myocardial Infarction via Histone Lysine β-Hydroxybutyrylation of CPT1A.JACC. Basic to translational science · 2025Article
- Smoking aggravates neovascular age-related macular degeneration via Sema4D-PlexinB1 axis-mediated activation of pericytes.Nature communications · 2025Article
- Elucidating molecular pathogenesis and developing targeted therapeutic interventions for cerebrovascular endothelial cell-mediated vascular dementia.Frontiers in aging neuroscience · 2025Review
- Predictive value of liver and kidney function and bone metabolism markers for postoperative outcomes in diabetic retinal surgery.American journal of translational research · 2025Article
- Protein O-GlcNAcylation coupled to Hippo signaling drives vascular dysfunction in diabetic retinopathy.Nature communications · 2024Article
- Ginsenoside RbChinese herbal medicines · 2024Review
- A feedback loop driven by H3K9 lactylation and HDAC2 in endothelial cells regulates VEGF-induced angiogenesis.Genome biology · 2024Article
- Orchestrating Resilience: How Neuropilin-2 and Macrophages Contribute to Cardiothoracic Disease.Journal of clinical medicine · 2024Review
- Mechanism of action ofHeliyon · 2024Article
- Evaluation of BR1 and BI30 AAVs for Brain Endothelial Tropism.ASN neuro · 2024Article
- Single-cell transcriptomic analysis of gingivo-buccal oral cancer reveals two dominant cellular programs.Cancer science · 2023Article
Corrections and comments
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Authors and funding
12 authors at 6 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Abnormal angiogenesis and regression of the diseased retinal vasculature are key processes associated with ischemic retinopathies, but the underlying mechanisms that regulate vascular remodeling remain poorly understood. Here, we confirmed the specific expression of semaphorin 3G (Sema3G) in retinal endothelial cells (ECs), which was required for vascular remodeling and the amelioration of ischemic retinopathy. We found that Sema3G was elevated in the vitreous fluid of patients with proliferative diabetic retinopathy (PDR) and in the neovascularization regression phase of oxygen-induced retinopathy (OIR). Endothelial-specific Sema3G knockout mice exhibited decreased vessel density and excessive matrix deposition in the retinal vasculature. Moreover, loss of Sema3G aggravated pathological angiogenesis in mice with OIR. Mechanistically, we demonstrated that HIF-2α directly regulated Sema3G transcription in ECs under hypoxia. Sema3G coordinated the functional interaction between β-catenin and VE-cadherin by increasing β-catenin stability in the endothelium through the neuropilin-2 (Nrp2)/PlexinD1 receptor. Furthermore, Sema3G supplementation enhanced healthy vascular network formation and promoted diseased vasculature regression during blood vessel remodeling. Overall, we deciphered the endothelium-derived Sema3G-dependent events involved in modulating physiological vascular remodeling and regression of pathological blood vessels for reparative vascular regeneration. Our findings shed light on the protective effect of Sema3G in ischemic retinopathies.
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