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Published on: June 3, 2018
Transcriptomic Atlas of Human Trabecular Meshwork Uncovers the Cellular Landscape and Provides Insights into Glaucoma
Gulab Zode1, Prakadeeswari Gopalakrishnan2, Pei Tan3
1UCI.
Research Square
|July 3, 2026
Summary
Glaucoma damages the trabecular meshwork (TM), affecting eye pressure. This study reveals cell-specific molecular changes in TM cells from glaucoma patients, identifying new therapeutic targets for vision loss.
Area of Science:
- Ophthalmology
- Genomics
- Cell Biology
Background:
- The trabecular meshwork (TM) is crucial for regulating intraocular pressure (IOP) by controlling aqueous humor outflow.
- Dysfunction of the TM is a primary cause of glaucoma, a leading cause of vision loss.
- Understanding cellular and molecular alterations in the human TM during glaucoma is essential for developing effective treatments.
Purpose of the Study:
- To create a comprehensive single-nucleus transcriptomic atlas of the human TM in normal and glaucomatous eyes.
- To identify distinct cell populations within the TM and characterize their transcriptomic profiles.
- To elucidate cell-type-specific molecular changes associated with glaucoma in the TM.
Main Methods:
- Single-nucleus RNA sequencing (snRNA-seq) was performed on human TM tissues from normal and glaucomatous eyes.
- Computational analysis was used to identify and classify distinct cell populations within the TM.
- Comparative transcriptomic analysis was conducted to identify differentially expressed genes and pathways in glaucoma.
Main Results:
- Analysis of 285,356 nuclei identified 17 distinct cell populations, including TM structural subtypes, endothelial, neural-associated, and immune cells.
- Glaucoma was associated with widespread, cell-type-specific transcriptomic remodeling in the TM.
- Key altered pathways included metal ion homeostasis, inflammation, calcium signaling, autophagy, extracellular matrix regulation, and stress responses.
Conclusions:
- Glaucoma induces a coordinated multicellular remodeling program in the TM, involving proteostasis failure, mitochondrial dysfunction, inflammation, and fibrosis.
- Fibroblast and myofibroblast-like TM cells show signatures of fibrotic remodeling, potentially contributing to increased outflow resistance.
- These findings highlight cell-type-specific therapeutic targets for restoring TM function and preventing vision loss in glaucoma.
