昆明医科大学学报2025，Vol.46Issue(11)：35-42,8.DOI:10.12259/j.issn.2095-610X.S20251105
miR-23通过调控PI3K/AKT/mTOR通路改善高血压性心力衰竭大鼠心肌血管生成的机制
The Mechanism of miR-23 Regulating PI3K/AKT/mTOR Pathway to Improve Myocardial Angiogenesis in Hypertensive Heart Failure Rats
摘要
Abstract
Objective To investigate the mechanisms by which miR-23 regulates the PI3K/AKT/mTOR signaling pathway to influence myocardial remodeling,fibrosis,and angiogenesis in hypertensive heart failure(HF)rats.Methods Forty rats were randomly divided into four groups(n=10 per group):a control group,a model group,an antagomir-NC group,and an antagomir-23 group.The HF model was established using a high-salt diet,and intervention was performed via tail vein injection of antagomir-23.Cardiac function parameters,the degree of myocardial fibrosis,cell apoptosis levels,and the expression of angiogenesis-related proteins including CD31,VEGF,and bFGF were measured in each group.Concurrently,the activity of the PI3K/AKT/mTOR signaling pathway was assessed.A dual-luciferase reporter assay was conducted to confirm that miR-23 targets PI3K.Results Inhibition of miR-23 significantly improved cardiac function in hypertensive HF rats,reduced myocardial fibrosis and apoptosis,and enhanced the expression of CD31,VEGF,bFGF,and activated the PI3K/AKT/mTOR signaling pathway in hypertensive HF rats(all P<0.05).The dual-luciferase assay confirmed that miR-23 negatively regulates PI3K expression.Conclusion Inhibition of miR-23 can activate the PI3K/AKT/mTOR signaling pathway,promote angiogenesis,reduce myocardial damage,thereby delaying the progression of hypertensive heart failure.关键词
高血压/心力衰竭/miR-23/心肌重构/纤维化/血管生成Key words
Hypertension/Heart failure/miR-23/Myocardial remodeling/Fibrosis/Angiogenesis分类
医药卫生引用本文复制引用
张海行,张敬云,许丹丹,曹路,李晶晶..miR-23通过调控PI3K/AKT/mTOR通路改善高血压性心力衰竭大鼠心肌血管生成的机制[J].昆明医科大学学报,2025,46(11):35-42,8.基金项目
河北省医学科学研究课题计划项目(20242389) （20242389）
