Volume 46 Issue 11
Nov.  2025
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Haixing ZHANG, Jingyun ZHANG, Dandan XU, Lu CAO, Jingjing LI. The Mechanism of miR-23 Regulating PI3K/AKT/mTOR Pathway to Improve Myocardial Angiogenesis in Hypertensive Heart Failure Rats[J]. Journal of Kunming Medical University, 2025, 46(11): 35-42. doi: 10.12259/j.issn.2095-610X.S20251105
Citation: Haixing ZHANG, Jingyun ZHANG, Dandan XU, Lu CAO, Jingjing LI. The Mechanism of miR-23 Regulating PI3K/AKT/mTOR Pathway to Improve Myocardial Angiogenesis in Hypertensive Heart Failure Rats[J]. Journal of Kunming Medical University, 2025, 46(11): 35-42. doi: 10.12259/j.issn.2095-610X.S20251105

The Mechanism of miR-23 Regulating PI3K/AKT/mTOR Pathway to Improve Myocardial Angiogenesis in Hypertensive Heart Failure Rats

doi: 10.12259/j.issn.2095-610X.S20251105
  • Received Date: 2025-04-10
    Available Online: 2025-11-06
  • Publish Date: 2025-11-25
  •   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.
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