Related Experiment Video
Updated: Aug 7, 2026

05:03
Establishing a Silicosis Rat Model via Exposure of Whole-Body to Respirable Silica
Published on: October 28, 2022
1.2K
Silicone Oil Affects Fibrosis of Human Trabecular Meshwork Cells by Upregulating Ferroptosis Through a ROS/NOX4/Smad3
Jing Wang1, Yang Zhang1, Huimin Zhong2
1Department of Ophthalmology, Ruijin Hospital Affiliated Medical School, Shanghai Jiaotong University, Shanghai, China.
Investigative Ophthalmology & Visual Science
|March 11, 2025
Summary
Silicone oil (SiO) can cause secondary glaucoma by damaging trabecular meshwork cells. This study reveals ferroptosis and the ROS/NOX4/Smad3 pathway are key mechanisms, offering targets to prevent complications.
Area of Science:
- Ophthalmology
- Cell Biology
- Biochemistry
Background:
- Silicone oil (SiO) is crucial for retinal reattachment in complex cases.
- Secondary glaucoma is a significant complication of intravitreal SiO tamponade.
- Trabecular meshwork cells (HTMCs) are vital for regulating intraocular pressure.
Purpose of the Study:
- To investigate the effects of SiO on HTMCs.
- To elucidate the mechanisms underlying SiO-induced ocular complications.
- To identify potential therapeutic targets for mitigating SiO-related adverse effects.
Main Methods:
- Co-culture of HTMCs with SiO.
- Assessment of cell proliferation, fibrosis markers, and ferroptosis.
- Gene knockdown of NOX4 and Smad3 to explore underlying pathways.
Main Results:
- SiO inhibited HTMC proliferation and increased fibrosis markers.
- SiO elevated ferroptosis levels in HTMCs.
- NOX4 upregulation and Smad3 activation mediated SiO-induced ferroptosis and ROS increase.
Conclusions:
- Ferroptosis and the ROS/NOX4/Smad3 axis are critical in SiO-induced intraocular pressure elevation.
- These findings offer insights into potential therapeutic strategies.
- Mitigating postoperative complications associated with SiO tamponade is a key goal.
More Related Videos
Related Concept Videos
Protein Modifications in the RER
Modification of secretory and transmembrane proteins entering the rough ER begins in the ER lumen. These modifications aid in protein folding and stabilize the acquired tertiary structure. Protein modifications in the rough ER co-occur at different stages of protein folding.
Broadly, these modifications can be categorized into four main categories — glycosylation, formation of disulfide bonds, assembly of protein subunits, and specific proteolytic cleavages like removal of signal sequences.
Broadly, these modifications can be categorized into four main categories — glycosylation, formation of disulfide bonds, assembly of protein subunits, and specific proteolytic cleavages like removal of signal sequences.
Necrosis
Necrosis is considered as an “accidental” or unexpected form of cell death that ends in cell lysis. The first noticeable mention of “necrosis” was in 1859 when Rudolf Virchow used this term to describe advanced tissue breakdown in his compilation titled “Cell Pathology”.
Morphological Manifestations of Necrosis
Necrotic cells show different types of morphological appearance depending on the type of tissue and infection. In coagulative necrosis, cells become anucleated and die, but their...
Morphological Manifestations of Necrosis
Necrotic cells show different types of morphological appearance depending on the type of tissue and infection. In coagulative necrosis, cells become anucleated and die, but their...

