Targeting the neurovascular unit in retinal fibrosis: mechanisms and therapeutic perspectives

TL;DR

This paper reviews how retinal fibrosis develops and explores new ways to treat it by focusing on the neurovascular unit and fibrotic mechanisms.

Contribution

The paper provides a systematic review of retinal fibrosis mechanisms and therapeutic targets from the perspective of the neurovascular unit.

Findings

Retinal fibrosis involves myofibroblast activation and extracellular matrix deposition.

Key mechanisms include epithelial mesenchymal transition and macrophage/pericyte-to-myofibroblast transitions.

The neurovascular unit plays a central role in fibrotic processes, offering potential therapeutic targets.

Abstract

Retinal fibrosis, a severe complication observed in conditions like age-related macular degeneration and diabetic retinopathy, characterized by aberrant myofibroblast activation and excessive extracellular matrix (ECM) deposition, which ultimately led to irreversible visual impairment. Currently, the mechanisms underlying retinal fibrosis remain unclear and existing treatments remain incompletely understood. Thus, a comprehensive understanding of disease mechanisms, together with the development of innovative therapeutic approaches, is essential for advancing effective treatment strategies. This review systematically examines the pathogenesis of retinal fibrosis from the perspective of the neurovascular unit (NVU), with a particular focus on the roles of endothelial cells, pericytes, and glial cells in fibrotic processes. It highlights key fibrotic mechanisms, including epithelial mesenchymal transition (EMT) as well as macrophage and pericyte-to-myofibroblast transitions (MMT/PMT). It further analyzes the molecular mechanisms that regulate myofibroblast activation and extracellular matrix deposition. Additionally, this review outlines potential therapeutic targets for the treatment of retinal fibrosis.

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