The Mechanism of miR-23 Regulating PI3K/AKT/mTOR Pathway to Improve Myocardial Angiogenesis in Hypertensive Heart Failure Rats
10.12259/j.issn.2095-610X.S20251105
- VernacularTitle: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
- Author:
Haixing ZHANG
1
;
Jingyun ZHANG
;
Dandan XU
;
Lu CAO
;
Jingjing LI
Author Information
1. 定州市人民医院心内科,河北 保定 073000
- Keywords:
Hypertension;
Heart failure;
miR-23;
Myocardial remodeling;
Fibrosis;
Angiogenesis
- From:
Journal of Kunming Medical University
2025;46(11):35-42
- CountryChina
- Language:Chinese
-
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.
