New Gene Targets for Diagnosis and Therapy of Diabetic Retinopathy

用于诊断和治疗糖尿病视网膜病变的新基因靶点

阅读:1

Abstract

Objective: Diabetic retinopathy (DR), considered one of the most common microvascular complications associated with diabetes mellitus (DM), involves both neuronal and vascular dysfunctions in the retina. Neuronal damage and vision loss occur progressively in patients with DR. A number of genetic targets have been identified for DR and gene-related treatments as well as early diagnostic techniques have been developed. Despite some medical advances, DR remains a devastating complication of diabetes. This study aimed to identify new gene targets that can be used for the prognosis and treatment of DR.. Materials and Methods: Eight candidate genes were analyzed using Synergy Brands Green (SYBR-green)- based real-time polymerase chain reaction in peripheral blood mononuclear cells (PBMCs) from 45 individuals: DR patients (n=15), DM patients without DR (n=15), and healthy controls (n=15). STRING v11 was used for protein-protein interaction analysis. Gene expression differences were evaluated using ANOVA, with significance set at P < .05. Results: HIF1A and VEGFA were significantly upregulated in both DR and DM groups compared to controls (HIF1A: fold change 5.28; VEGFA: fold change 5.20 for DR group). SERPING1 was specifically upregulated in DR patients (fold change 3.42). CX3CR1 and BDNF were downregulated in both DR and DM groups (CX3CR1: fold change 8.32; BDNF: fold change 3.21), while IGFBP3 was significantly downregulated only in DR patients (fold change 6.5). STRING analysis revealed strong interactions between SERPING1 and complement pathway components, while IGFBP3 was linked to insulin-like growth factor signaling. Conclusion: In light of these findings, we observed that SERPING1 and IGFBP3 genes might be proposed as targets for early diagnosis and treatment for DR.

特别声明

1、本页面内容包含部分的内容是基于公开信息的合理引用;引用内容仅为补充信息,不代表本站立场。

2、若认为本页面引用内容涉及侵权,请及时与本站联系,我们将第一时间处理。

3、其他媒体/个人如需使用本页面原创内容,需注明“来源:[生知库]”并获得授权;使用引用内容的,需自行联系原作者获得许可。

4、投稿及合作请联系:info@biocloudy.com。