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Updated: Sep 6, 2025

Author Spotlight: Unraveling the Molecular Mechanisms in PCO and Fibrosis Following Cataract Surgery
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Author Spotlight: Unraveling the Molecular Mechanisms in PCO and Fibrosis Following Cataract Surgery

Published on: December 1, 2023

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Toll-like receptor 3 gene regulates cataract-related mechanisms via the Jagged-1/Notch signaling pathway

Weiwei Xie1, Qihua Yu1, Layi Wang1

  • 1Department of Ophthalmology, The Affiliated Ningbo Eye Hospital of Wenzhou Medical University, Ningbo, Zhejiang, China.

Bioengineered
|June 27, 2022
PubMed

Insights

Toll-like receptor (TLR) 3 activation inhibits lens epithelial cell proliferation and migration, preventing fibrosis and posterior capsule opacification. This discovery highlights the TLR3-Jagged-1/Notch pathway as a potential therapeutic target for fibrotic cataracts.

Area of Science:

  • Ophthalmology
  • Cell Biology
  • Immunology

Background:

  • Epithelial-mesenchymal transition (EMT) drives organ fibrosis and is implicated in cataract pathogenesis.
  • Posterior capsule opacification (PCO) is a common complication following cataract surgery, often linked to fibrosis.

Purpose of the Study:

  • To investigate the role of Toll-like receptor (TLR) 3 in transforming growth factor-beta 2 (TGF-β2)-induced EMT in lens epithelial cells (LECs).
  • To elucidate the molecular mechanism by which TLR3 influences LEC behavior and fibrosis.
  • To identify potential therapeutic targets for fibrotic cataracts and PCO.

Main Methods:

  • Human LEC line (SRA01/04) treated with TGF-β2 in the presence or absence of TLR3.
  • Cell proliferation, migration, and invasion assessed using CCK-8 and Transwell assays.
  • Protein and RNA expression analyzed via Western blotting and qPCR.
  • Functional gain and loss studies performed.

Main Results:

  • TLR3 modulates the proliferation, migration, and invasion of LECs.
  • TLR3 regulates TGF-β2-induced EMT in LECs.
  • TLR3 influences the expression of Jagged-1, Notch-1, and Notch-3, indicating regulation of the Jagged-1/Notch signaling pathway.

Conclusions:

  • TLR3 plays a protective role against lens fibrosis by inhibiting TGF-β2-induced EMT via the Jagged-1/Notch signaling pathway.
  • The TLR3-Jagged-1/Notch signaling axis represents a promising therapeutic target for treating fibrotic cataracts and preventing PCO.
Keywords:
EMTJagged-1/Notch signaling pathwayTLR3fibrotic cataract

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