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Related Experiment Video

Updated: Apr 23, 2026

A Magnetic Microbead Occlusion Model to Induce Ocular Hypertension-Dependent Glaucoma in Mice
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TXNDC5 in POAG: Promoting Extracellular Matrix Protein Accumulation and Raising Intraocular Pressure.

Dan Song1,2,3, Lixin Wen1,2,3, Mingmin Hou1,2,3

  • 1Department of Ophthalmology, Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.

Investigative Ophthalmology & Visual Science
|April 21, 2026
PubMed
Summary

Targeting TXNDC5, a protein linked to extracellular matrix buildup in the eye, may offer a new treatment for primary open-angle glaucoma (POAG) by lowering intraocular pressure (IOP).

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Area of Science:

  • Ophthalmology
  • Cell Biology
  • Molecular Biology

Background:

  • Primary open-angle glaucoma (POAG) is characterized by increased intraocular pressure (IOP) due to extracellular matrix (ECM) accumulation in the trabecular meshwork (TM).
  • Current treatments for POAG do not effectively target the underlying mechanism of ECM accumulation.
  • Identifying key proteins involved in TM ECM accumulation is crucial for developing novel therapeutic strategies.

Purpose of the Study:

  • To identify key proteins contributing to TM ECM accumulation in POAG.
  • To elucidate the mechanism by which TXNDC5 influences TM ECM accumulation and IOP.
  • To explore TXNDC5 as a potential therapeutic target for POAG.

Main Methods:

  • Label-free quantitative proteomics to screen for upregulated proteins in TGFβ2-induced TM cells.
  • Validation of TXNDC5 and ECM protein interactions using qPCR, Western blot, and immunohistochemistry.
  • Investigation of TXNDC5 degradation via molecular chaperone-mediated autophagy (CMA) and its modulation by autophagy inhibitors.

Main Results:

  • TXNDC5 was found to increase ECM accumulation in human TM cells by upregulating TGFβ R2 expression.
  • TXNDC5 is degraded through the CMA pathway, and AR7 treatment reversed TGFβ2-induced TM ECM accumulation.
  • In vivo knockdown of TXNDC5 reduced ECM accumulation and ocular hypertension in a mouse model.

Conclusions:

  • TXNDC5 plays a significant role in TM ECM accumulation and IOP elevation in POAG.
  • Targeting elevated TXNDC5 levels presents a promising therapeutic avenue for POAG.
  • Further research into TXNDC5 modulation could lead to effective treatments for POAG by reducing TM ECM protein buildup.