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Updated: Aug 13, 2026
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Toxicity Screens in Human Retinal Organoids for Pharmaceutical Discovery
Published on: March 4, 2021
Clodronate Liposome effectively Mitigates Chemically-Induced Retinal Pigment Epithelium Toxicity
Zixiang Wang1, Xinyuan Yu2, Yilong Shi2
1Department of Emergency Medicine, The Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University, Wenzhou, 325027, China; National Engineering Research Center of Ophthalmology and Optometry, Eye Hospital, Wenzhou Medical University, Wenzhou, 325027, China.
Experimental Eye Research
|August 11, 2026
Summary
Peripheral macrophage depletion protected against chemical-induced retinal damage in one model, but not another. This suggests clodronate liposomes offer model-dependent protection against vision loss from eye injury.
Area of Science:
- Ophthalmology
- Neuroscience
- Toxicology
Background:
- Chemical-induced retinal degeneration poses a significant clinical challenge with limited treatment options.
- Microglia and peripheral macrophages are implicated in retinal degenerative diseases, suggesting potential therapeutic targets.
Purpose of the Study:
- To investigate the efficacy of targeting myeloid cells, specifically microglia and macrophages, in mitigating chemical-induced retinal damage.
- To evaluate the protective effects of minocycline, PLX3397, and clodronate liposomes in sodium iodate (NaIO3) and N-methyl-N-nitrosourea (MNU) retinal degeneration models.
Main Methods:
- Systematic evaluation of minocycline (microglial activation inhibitor), PLX3397 (microglial depletor), and clodronate liposomes (peripheral macrophage depletor) in NaIO3 and MNU rodent models.
- Assessment of retinal damage through funduscopy, electroretinography (ERG), and photoreceptor apoptosis assays.
Main Results:
- Minocycline and PLX3397 failed to protect against retinal damage in both models.
- Clodronate liposomes significantly reduced retinal atrophy and improved visual function in the NaIO3 model.
- Clodronate liposomes did not provide protection in the MNU model, indicating model-specific effects.
Conclusions:
- Targeting resident microglia is ineffective for preventing chemical-induced retinal degeneration.
- Peripheral macrophage depletion demonstrates therapeutic potential in specific models of retinal injury, suggesting a role in modulating retinal pigment epithelium (RPE) toxicity.
