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Updated: Sep 10, 2025

In Vitro and In Vivo Models to Study Corneal Endothelial-mesenchymal Transition
Published on: August 20, 2016
Bioinformatic Analysis of the Value of Mitophagy and Immune Responses in Corneal Endothelial Dysfunction
Ruilin Guo1, Chenjia Xu2, Yi Yu1
1State Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Sun Yat-sen University, Guangdong Provincial Key Laboratory of Ophthalmology and Visual Science, Guangzhou 510060, China.
Abstract:
This study was conducted to elucidate the mitophagy-related differentially expressed genes (MRDEGs) in corneal endothelial dysfunction (CED) and to identify key hub genes that could provide insights into the disease pathogenesis and potential targeted therapies. To achieve this, CED models were established in female SD rats, and RNA sequencing of coronal endothelium samples was conducted to generate a self-testing dataset. Comprehensive bioinformatics analyses were executed, which included the identification of differentially expressed genes (DEGs), GO and KEGG enrichment analyses, GSEA, and GSVA. A protein-protein interaction (PPI) network was constructed to identify highly interconnected hub genes, followed by the construction of ROC curves to validate MRDEGs within the dataset, alongside qRT-PCR assays. Our findings revealed a total of 18,511 DEGs, among which 20 genes were characterized as MRDEGs. Enrichment analyses indicated significant associations with monocyte differentiation and lymphocyte proliferation. Importantly, eight hub genes emerged from the PPI network as promising therapeutic targets. In conclusion, this study underscores the important role of MRDEGs and immune infiltration in CED, laying the groundwork for future investigations into targeted therapies for this disease.
Insights
This study identified mitophagy-related genes in corneal endothelial dysfunction (CED), revealing immune cell roles and eight potential therapeutic targets for this eye condition.
Area of Science:
- Ophthalmology
- Molecular Biology
- Genetics
Background:
- Corneal endothelial dysfunction (CED) is a significant cause of vision impairment.
- Understanding the molecular mechanisms underlying CED is crucial for developing effective treatments.
Purpose of the Study:
- To identify mitophagy-related differentially expressed genes (MRDEGs) in CED.
- To pinpoint key hub genes for potential targeted therapies.
- To explore the role of immune infiltration in CED pathogenesis.
Main Methods:
- Establishment of CED rat models and RNA sequencing of corneal endothelium.
- Bioinformatics analyses including DEG identification, GO/KEGG enrichment, GSEA, and GSVA.
- Protein-protein interaction (PPI) network construction, ROC curve analysis, and qRT-PCR validation.
Main Results:
- 18,511 differentially expressed genes (DEGs) were identified, with 20 classified as MRDEGs.
- Enrichment analyses highlighted associations with monocyte differentiation and lymphocyte proliferation.
- Eight hub genes were identified as potential therapeutic targets for CED.
Conclusions:
- MRDEGs and immune cell infiltration play a critical role in CED.
- The identified hub genes offer promising avenues for future targeted therapeutic strategies.
- This research provides a foundation for further investigation into CED treatment.
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