Fibrotic Remodeling in Retinal Vascular Diseases: Cellular Origins, Molecular Mechanisms, and Therapeutic Perspectives.
- 1Department of Pharmacology and Regenerative Medicine, University of Illinois College of Medicine, Chicago, IL 60612, USA.
- 2Department of Ophthalmology and Visual Sciences, University of Illinois College of Medicine, Chicago, IL 60612, USA.
Abstract
Fibrosis is a major vision-threatening complication of neovascular retinal diseases, including neovascular age-related macular degeneration (nAMD) and proliferative diabetic retinopathy (PDR). Although vascular endothelial growth factor (VEGF) inhibition effectively suppresses vascular leakage and neovascularization, some patients still develop fibrosis and experience irreversible vision loss. Recent studies have identified multiple interconnected signaling pathways that contribute to fibrotic progression, highlighting the potential need for combination or multitargeted therapeutic strategies. This review summarizes the cellular origins of myofibroblasts, the molecular mechanisms underlying fibrosis, and recent advances in antifibrotic therapies. We particularly highlight the angio-fibrotic switch, mesenchymal transition, cellular stress responses, extracellular matrix remodeling, mechanotransduction, and emerging therapeutic approaches for ocular fibrosis. Relevant preclinical and clinical studies were identified through searches of PubMed and clinical trial registries.
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BibTeX
@article{ning2026fibrotic,
title = {{Fibrotic Remodeling in Retinal Vascular Diseases: Cellular Origins, Molecular Mechanisms, and Therapeutic Perspectives.}},
author = {Jia Yu Ning and Brian Wang and Miyuki Ishida Yamamoto and Kaori H Yamada},
journal = {Cells},
year = {2026},
month = sep,
doi = {10.3390/cells15191772},
url = {https://europepmc.org/article/MED/42882470},
note = {CC BY},
}
RIS
TY - JOUR
TI - Fibrotic Remodeling in Retinal Vascular Diseases: Cellular Origins, Molecular Mechanisms, and Therapeutic Perspectives.
AU - Jia Yu Ning
AU - Brian Wang
AU - Miyuki Ishida Yamamoto
AU - Kaori H Yamada
PY - 2026
DA - 2026/09/29
JO - Cells
DO - 10.3390/cells15191772
UR - https://europepmc.org/article/MED/42882470
AB - Fibrosis is a major vision-threatening complication of neovascular retinal diseases, including neovascular age-related macular degeneration (nAMD) and proliferative diabetic retinopathy (PDR). Although vascular endothelial growth factor (VEGF) inhibition effectively suppresses vascular leakage and neovascularization, some patients still develop fibrosis and experience irreversible vision loss. Recent studies have identified multiple interconnected signaling pathways that contribute to fibrotic progression, highlighting the potential need for combination or multitargeted therapeutic strategies. This review summarizes the cellular origins of myofibroblasts, the molecular mechanisms underlying fibrosis, and recent advances in antifibrotic therapies. We particularly highlight the angio-fibrotic switch, mesenchymal transition, cellular stress responses, extracellular matrix remodeling, mechanotransduction, and emerging therapeutic approaches for ocular fibrosis. Relevant preclinical and clinical studies were identified through searches of PubMed and clinical trial registries.
SN - 2073-4409
ER -