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PRRX1 Orchestrates Pericyte-Myofibroblast Transition in Pathological Retinal Fibrosis
Zhishang Meng1, Dan Liu1, Yuqian Hu1
1Department of Ophthalmology, The Second Xiangya Hospital, Central South University, Changsha, China.
Investigative Ophthalmology & Visual Science
|November 13, 2025
Summary
Paired box 1 (PRRX1) drives retinal fibrosis by promoting pericyte-myofibroblast transition. Silencing PRRX1 reduces fibrosis, suggesting it as a therapeutic target for retinal fibrotic diseases.
Area of Science:
- Ophthalmology
- Cell Biology
- Molecular Medicine
Background:
- Retinal fibrosis is a major cause of vision loss.
- Pericyte-myofibroblast transition is a key process in fibrosis.
- The role of PRRX1 in retinal fibrosis is not well understood.
Purpose of the Study:
- To investigate the role of PRRX1 in pericyte-myofibroblast transition.
- To determine PRRX1's contribution to pathological retinal fibrosis.
Main Methods:
- Transcriptomic profiling of human and murine retinal tissues.
- Single-cell RNA sequencing to identify PRRX1-expressing pericyte subpopulations.
- In vitro studies using primary pericytes under hypoxia with PRRX1 knockdown.
- In vivo studies using a laser-induced choroidal neovascularization model.
Main Results:
- PRRX1 was upregulated in fibrotic retinal tissues and enriched in transitioning pericytes.
- PRRX1 knockdown reduced fibrotic gene expression and migration in vitro.
- PRRX1 silencing decreased subretinal fibrosis and neovascularization in vivo.
Conclusions:
- PRRX1 is a key regulator of pericyte-mediated fibrotic remodeling in the retina.
- Targeting PRRX1 presents a potential therapeutic strategy for retinal fibrosis.
