Gu Ping, Yu Dan, Zhang Yu, Chai Xiaoying
Department of Endocrinology, Affiliated Hospital of Jiangnan University, Wuxi, People's Republic of China.
Diabetes Metab Syndr Obes. 2025 Sep 4;18:3237-3247. doi: 10.2147/DMSO.S542183. eCollection 2025.
This study aims to explore the clinical significance of miR-17-5p in T2DM and its chronic complications.
A total of 100 patients with T2DM and 90 healthy controls were included. The expression of miR-17-5p was detected by reverse transcription-polymerase chain reaction. A receiver operating characteristic curve was plotted to evaluate the diagnostic value of miR-17-5p for T2DM. Pearson correlation analysis was used to explore the correlation between miR-17-5p and blood glucose indicators in T2DM patients. The Kaplan-Meier curve and multivariate Cox regression analysis were employed to analyze the factors influencing chronic complications. Liposome-mediated transfection technology was used to transfect miR-17-5p mimics and inhibitors into endothelial progenitor cells (EPCs) respectively, to achieve overexpression and knockdown of miR-17-5p in cells. On this basis, we further investigate the potential molecular mechanism by which miR-17-5p is involved in the occurrence and development of chronic complications inT2DM.
Serum miR-17-5p was significantly downregulated in T2DM patients (vs healthy controls, P<0.001). The AUC for distinguishing T2DM patients from healthy individuals was 0.932. The expression of this miRNA was significantly negatively correlated with FBG (r=-0.718) and HbA1c (r=-0.695) (P<0.001). Follow-up showed that low expression of miR-17-5p was closely associated with T2DM chronic complications (complication group vs non-complication group, P<0.001), with an AUC of 0.866 for distinguishing the presence from the absence of complications. Kaplan-Meier analysis indicated that individuals with low miR-17-5p expression had a higher risk of complications (Log-rank P=0.009). Mechanistically, miR-17-5p targets FBXO48 and affects the functions of EPCs.
The expression of miR-17-5p is reduced in T2DM. It influences the functions of EPCs by targeting , and may be involved in the occurrence and development of chronic complications of T2DM.
本研究旨在探讨miR-17-5p在2型糖尿病(T2DM)及其慢性并发症中的临床意义。
共纳入100例T2DM患者和90例健康对照者。采用逆转录-聚合酶链反应检测miR-17-5p的表达。绘制受试者工作特征曲线以评估miR-17-5p对T2DM的诊断价值。采用Pearson相关分析探讨T2DM患者中miR-17-5p与血糖指标之间的相关性。采用Kaplan-Meier曲线和多因素Cox回归分析来分析影响慢性并发症的因素。利用脂质体介导的转染技术分别将miR-17-5p模拟物和抑制剂转染至内皮祖细胞(EPCs)中,以实现细胞中miR-17-5p的过表达和敲低。在此基础上,我们进一步研究miR-17-5p参与T2DM慢性并发症发生发展的潜在分子机制。
T2DM患者血清miR-17-5p显著下调(与健康对照者相比,P<0.001)。区分T2DM患者与健康个体的曲线下面积(AUC)为0.932。该微小RNA的表达与空腹血糖(FBG,r=-0.718)和糖化血红蛋白(HbA1c,r=-0.695)显著负相关(P<~0.001)。随访显示,miR-17-5p低表达与T2DM慢性并发症密切相关(并发症组与无并发症组相比,P<0.001),区分有无并发症的AUC为0.866。Kaplan-Meier分析表明,miR-17-5p低表达个体发生并发症的风险更高(对数秩检验P=0.009)。机制上,miR-17-5p靶向FBXO48并影响EPCs的功能。
T2DM中miR-17-5p表达降低。它通过靶向作用影响EPCs的功能,可能参与T2DM慢性并发症的发生发展。