ArticleNature communications2025
Endothelial protein C receptor promotes retinal neovascularization through heme catabolism.
Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed.
- FLVCR2 Regulation of Intracellular Heme Modulates Vascular Tip/Stalk Specification During Retinal Angiogenesis.Investigative ophthalmology & visual science · 2026Article
- More than a ring: the emerging role of heme in angiogenesis.Cell communication and signaling : CCS · 2026Review
- Dual-targeting VEGF and TNF-α with bispecific antibody eyedrops for synergistic treatment of uveitis.Journal of nanobiotechnology · 2026Article
- Functions of dendrobine in a zebrafish model of diabetic retinopathy.Journal of translational medicine · 2026Article
- Engineering Strategies of Colloidal Drug Delivery Systems, a Rising Star in Ocular Neovascular Diseases.Molecules (Basel, Switzerland) · 2026Review
- Genetic variants and serum biomarkers of CXCL8, MAP3K7, LTA/TNF, EXOC3L1, PROCR, and TRAF2 in Age-Related macular degeneration: associations with disease risk and therapeutic response.Scientific reports · 2026Article
- Exploiting porphyrin metabolism to inhibit angiogenesis.Angiogenesis · 2026Article
- Activated Protein C and the Retina: From Physiology to Therapeutic Potential.International journal of molecular sciences · 2026Review
- Multi-omics integrated analysis identifies causal risk factors and therapeutic targets for diabetic retinopathy.Journal of translational medicine · 2025Article
- Comparative analysis of global and Chinese trends in the burden of ischemic stroke attributable to secondhand smoke from 1990-2021.Tobacco induced diseases · 2025Article
Corrections and comments
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Authors and funding
20 authors.
Funding
Abstract
Pathological retinal neovascularization (RNV) is one of the leading causes of blindness worldwide; however, its underlying mechanism remains unclear. Here, we found that the expression of endothelial protein C receptor (Epcr) was increased during RNV, and its ligand was elevated in the serum or vitreous body of patients with proliferative diabetic retinopathy. Deleting endothelial Epcr or using an EPCR-neutralizing antibody ameliorated pathological retinal angiogenesis. EPCR promoted endothelial heme catabolism and carbon monoxide release through heme oxygenase 1 (HO-1). Inhibition of heme catabolism by deleting endothelial Ho-1 or using an HO-1 inhibitor suppressed pathological angiogenesis in retinopathy. Conversely, supplementation with carbon monoxide rescued the angiogenic defects after endothelial Epcr or Ho-1 deletion. Our results identified EPCR-dependent endothelial heme catabolism as an important contributor to pathological angiogenesis, which may serve as a potential target for treating vasoproliferative retinopathy.
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Registered trials
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