School of Pharmacology, Binzhou Medical University, Guanhai Rd 346, Yantai, 264003, China.
Shandong Technology Innovation Center of Molecular Targeting and Intelligent Diagnosis and Treatment, Yantai, 264003, China.
Sci Rep. 2023 Aug 25;13(1):13956. doi: 10.1038/s41598-023-41194-2.
Corneal keratoconus (KC) is a dilated (ectatic) corneal disease characterized by a central thinning of the cornea, which causes protrusion into a conical shape that seriously affects vision. However, due to the complex etiology of keratoconus, its entire mechanism remains unclear and there is no mechanism-directed treatment method. Ferroptosis is a novel programmed cell death mechanism related to lipid peroxidation, stress, and amino acid metabolism, which plays a crucial role in various diseases. This study aimed to explore the relationship between keratoconus and ferroptosis, to provide new insights into the mechanism of keratoconus development, and potential treatment options based on further elucidation of this mechanism. The corresponding mRNA microarray expression matrix data of KC patients were obtained from GEO database (GSE204791). Weighted co-expression network analysis (WGCNA) and support vector machine recursive feature elimination (SVM-RFE) were selected to screen hub genes, which were overlapped with ferroptosis genes (FRGs) from FerrDb. GO and GSEA were performed to analyze differential pathways, ssGSEA was used to determine immune status, and then, feasible drugs were predicted by gene-drug network. Additionally, we predicted the miRNA and IncRNA of hub genes to identify the underlying mechanism of disease so as to predict treatment for the disease. The epithelial transcriptome from keratoconus tissue mRNA microarray data (GSE204791) was extracted for the main analysis, including eight epithelial cells and eight epithelial control cells. The differential genes that were overlapped by WGCAN, SVM-RFE and FRGs were mainly related to oxidative stress, immune regulation, cellular inflammation, and metal ion transport. Through further analysis, aldo-keto reductase family 1 member C3 (AKR1C3) was selected, and negatively correlated with mature CD56 natural killer (NK) cells and macrophages. Then, gene-drug interaction network analysis and miRNA prediction were performed through the website. It was concluded that four immune-related drugs (INDOMETHACIN, DAUNORUBICIN, DOXORUBICIN, DOCETAXEL) and a miRNA (has-miR-184) were screened to predict potential drugs and targets for disease treatment. To our knowledge, this was the first report of KC being associated with ferroptosis and prompted search for differential genes to predict drug targets of gene immunotherapy. Our findings provided insight and a solid basis for the analysis and treatment of KC.
角膜膨出症(KC)是一种扩张(扩张)的角膜疾病,其特征是角膜中央变薄,导致角膜向圆锥形突出,严重影响视力。然而,由于角膜膨出症的病因复杂,其整个机制仍不清楚,也没有针对该机制的治疗方法。铁死亡是一种与脂质过氧化、应激和氨基酸代谢有关的新型程序性细胞死亡机制,在各种疾病中起着至关重要的作用。本研究旨在探讨角膜膨出症与铁死亡之间的关系,为进一步阐明这一机制,为角膜膨出症的发展机制提供新的见解,并提供潜在的治疗选择。从 GEO 数据库(GSE204791)获得了 KC 患者的相应 mRNA 微阵列表达矩阵数据。选择加权共表达网络分析(WGCNA)和支持向量机递归特征消除(SVM-RFE)筛选枢纽基因,并与 FerrDb 中的铁死亡基因(FRGs)重叠。进行 GO 和 GSEA 分析差异通路,使用 ssGSEA 确定免疫状态,然后通过基因-药物网络预测可行的药物。此外,我们预测了枢纽基因的 miRNA 和 IncRNA,以确定疾病的潜在机制,从而预测疾病的治疗方法。从角膜膨出症组织 mRNA 微阵列数据(GSE204791)中提取上皮转录组进行主要分析,包括 8 个上皮细胞和 8 个上皮对照细胞。WGCAN、SVM-RFE 和 FRGs 重叠的差异基因主要与氧化应激、免疫调节、细胞炎症和金属离子转运有关。通过进一步分析,选择醛酮还原酶家族 1 成员 C3(AKR1C3),其与成熟 CD56 自然杀伤(NK)细胞和巨噬细胞呈负相关。然后,通过网站进行基因-药物相互作用网络分析和 miRNA 预测。结果筛选出四种免疫相关药物(INDOMETHACIN、DAUNORUBICIN、DOXORUBICIN、DOCETAXEL)和一个 miRNA(has-miR-184),以预测疾病治疗的潜在药物和靶点。据我们所知,这是 KC 与铁死亡相关的首次报道,并促使寻找差异基因以预测基因免疫治疗的药物靶点。我们的研究结果为 KC 的分析和治疗提供了新的见解和坚实的基础。