ArticleInvestigative ophthalmology & visual science2025
Transcriptomic Analysis of Human Lens Epithelium Tissue With and Without Cataract Surgery: Uncovering Novel Pathways of Post-Surgical Lens Epithelium Remodeling.
Article in Investigative ophthalmology & visual science, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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Who cites it
5 citing papers in PubMed.
- Lens aging and disease: Molecular mechanisms, functional consequences, and pharmacological implications.Progress in retinal and eye research · 2026Review
- Micheliolide suppresses epithelial-mesenchymal transition of lens epithelial cells via downregulating matrix metalloproteinase 8 to ameliorate posterior capsular opacification.Journal of translational medicine · 2026Article
- Case Report: Early bilateral capsular contraction syndrome associated with Epstein-Barr virus-positive uveitis after cataract surgery.Frontiers in medicine · 2026Article
- Artificial Intelligence in Ocular Transcriptomics: Applications of Unsupervised and Supervised Learning.Cells · 2025Review
- Unanswered questions regarding the pathogenesis of late onset posterior capsular opacification.Frontiers in ophthalmology · 2025Review
Corrections and comments
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Authors and funding
7 authors.
Funding
Abstract
Purpose: Cataract surgery is the most commonly performed ophthalmic procedure worldwide, yet long-term molecular adaptations of lens epithelial cells (LECs) following surgery remain poorly understood. Methods: We conducted bulk RNA sequencing on lens capsules from 34 human donors, including 17 with an average of 7 years post-cataract surgery and 17 non-cataract controls. Results: Differential expression analysis revealed substantial transcriptional changes in post-surgical LECs, including 1690 upregulated and 579 downregulated genes. Gene Set Enrichment Analysis (GSEA) and Gene Ontology (GO) identified activation of oxidative stress response, cell survival, and immune response signatures. Notably, genes involved in antioxidant defense (e.g. SOD2, GCLC, and TXN), anti-apoptotic regulation (BCL2L1 and XIAP), and DNA repair (ERCC1) were significantly upregulated in post-surgical samples. Immune-related genes (IL-8, CCL2, and TGFβ2) and complement components (C2 and C3) were elevated, suggesting persistent inflammatory signaling. Enrichment of TGF-β and Wnt/β-Catenin signaling, along with increased expression of epithelial mesenchymal transition (EMT) and fibrosis markers (ACTA2, FN1, and TNC), indicated long-term fibrotic remodeling. Senescence-associated genes (CDKN2A and CDKN1A) were also upregulated, whereas LMNB1 was downregulated, supporting a senescent phenotype in a subset of LECs. Immunofluorescence confirmed senescence and fibrosis at the protein level. GO enrichment and clustering revealed strong upregulation of cell migration, corroborated by elevated expression of migratory genes (ICAM1, VCAM1, and PLAU), suggesting acquisition of an invasive phenotype. Conclusions: Our findings reveal that LECs undergo sustained molecular reprogramming after cataract surgery, including inflammatory, fibrotic, migratory, and senescent changes. These adaptations may contribute to posterior capsule opacification (PCO) and highlight therapeutic targets for its prevention.
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