ArticleInvestigative ophthalmology & visual science2025
PRRX1 Orchestrates Pericyte-Myofibroblast Transition in Pathological Retinal Fibrosis.
Article in Investigative ophthalmology & visual science, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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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
2 citing papers in PubMed.
- A Primary Open-Angle Glaucoma Locus Near Transcription FactorOphthalmology science · 2026Article
- Targeting CDH13 as a therapeutic strategy to mitigate pathological ocular angiogenesis.Journal of translational medicine · 2026Article
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Authors and funding
11 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Purpose: To investigate the role of PRRX1 in pericyte-myofibroblast transition and its contribution to pathological retinal fibrosis. Methods: Transcriptomic profiling was conducted on human fibrovascular membranes and murine oxygen-induced retinopathy retinas to assess PRRX1 expression and its association with fibrosis-related genes. Single‑cell RNA sequencing was performed on retinal tissues to identify pericyte subpopulations and characterize PRRX1-driven molecular pathways. In vitro, primary mouse retinal pericytes underwent hypoxia with or without small interfering RNA-mediated PRRX1 knockdown to assess fibrotic gene expression and cell migration. In vivo, a laser-induced choroidal neovascularization model was used to assess the effect of PRRX1 silencing on subretinal fibrosis. Results: PRRX1 was significantly upregulated in both human fibrovascular membranes and oxygen-induced retinopathy retinas; single‑cell RNA sequencing revealed its enrichment in pericyte subpopulations undergoing pericyte-myofibroblast transition. PRRX1 knockdown reduced fibrotic gene expression and migratory activity in primary pericytes under hypoxia. In the choroidal neovascularization model, PRRX1 silencing significantly reduced subretinal fibrosis and neovascular lesion area. Conclusions: PRRX1 is a key regulator of pericyte-mediated fibrotic remodeling in the retina. Targeting PRRX1 offers a potential therapeutic approach for retinal fibrosis.
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Registered trials
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