Related Experiment Video
Updated: Jan 21, 2026

Mechanism of Kemeng Fang's Inhibition of Podocyte Apoptosis in Rats with Membranous Nephropathy through the PI3K/AKT Signaling Pathway
Published on: August 23, 2024
MiR-126 promotes endothelial cell apoptosis by targeting PI3K/Akt in rats with lower limb arteriosclerosis obliterans
1Department of Vascular Surgery, Zhongshan Hospital, Fudan University, Shanghai, China. fu.weiguo@zs-hospital.sh.cn.
Objective:
To investigate the influence of micro ribonucleic acid (miR)-126 on the rats with lower limb arteriosclerosis obliterans (ASO).
Materials And Methods:
Male Sprague- Dawley rats aged 3 months old were randomly divided into Sham operation group (Control group, n=10) and Model group (n=10), and the model of lower limb ASO was established. After modeling, the expression of miR-126 in arteries was detected using quantitative Real Time-Polymerase Chain Reaction (qRT-PCR), and the change in the downstream signaling pathway was examined via Western blotting. The human umbilical vein endothelial cells (HUVECs) were induced by oxidized low-density lipoprotein (Ox-LDL) to establish the model of endothelial injury, followed by detection of miR-126 expression. Then, the Luciferase assay was performed to verify the downstream target gene of miR-126. After being cultured, HUVECs were set as Control group, Ox-LDL induction group, and Ox-LDL + miR-126 inhibitor group, and the expressions of phosphorylated-protein kinase B (p-Akt) and cleaved cysteine-aspartic protease-3 (Caspase-3) were detected in the above groups.
Results:
After the establishment of the model, the expression level of miR-126 was raised in vessels, but the phosphatidylinositol 3-hydroxy kinase (PI3K)/Akt signals were weakened (p<0.01). Ox-LDL-induced endothelial cell apoptosis promoted the expression of miR-126, and the difference was statistically significant. The bioinformatics analysis results showed that PI3KR2 was a direct target of miR-126, which was also proven via the Luciferase assay. Moreover, the transfection with miR-126 inhibitor into endothelial cells suppressed Ox-LDL-induced cell apoptosis, thereby persistently activating the PI3K/Akt signaling pathway (p<0.01).
Conclusions:
In rats with lower limb arteriosclerosis obliterans (ASO), miR-126 represses the PI3K/Akt signaling pathway to accelerate endothelial cell apoptosis.
Insights
MicroRNA-126 (miR-126) exacerbates lower limb arteriosclerosis obliterans (ASO) by inhibiting the PI3K/Akt pathway, leading to increased endothelial cell apoptosis. Inhibiting miR-126 protects against ASO progression.
Area of Science:
- Vascular Biology
- Molecular Medicine
- Biochemistry
Background:
- Arteriosclerosis obliterans (ASO) is a significant cause of lower limb ischemia.
- The role of microRNAs in ASO pathogenesis requires further elucidation.
- Endothelial dysfunction is a key feature of ASO.
Purpose of the Study:
- To investigate the role of microRNA-126 (miR-126) in the development of lower limb arteriosclerosis obliterans (ASO) in a rat model.
- To explore the molecular mechanisms by which miR-126 influences endothelial cell apoptosis and the PI3K/Akt signaling pathway.
Main Methods:
- ASO model established in male Sprague-Dawley rats.
- miR-126 expression analyzed using qRT-PCR.
- PI3K/Akt signaling pathway assessed via Western blotting.
- Human umbilical vein endothelial cells (HUVECs) treated with oxidized low-density lipoprotein (Ox-LDL) to induce injury.
- Luciferase assay used to identify miR-126 targets.
Main Results:
- miR-126 expression was upregulated in ASO rat vessels, correlating with weakened PI3K/Akt signaling.
- Oxidized low-density lipoprotein (Ox-LDL) induced endothelial cell apoptosis and increased miR-126 expression.
- PI3K regulatory subunit 2 (PI3KR2) identified as a direct target of miR-126.
- Inhibition of miR-126 suppressed Ox-LDL-induced apoptosis and activated the PI3K/Akt pathway.
Conclusions:
- miR-126 plays a detrimental role in lower limb arteriosclerosis obliterans (ASO) by repressing the PI3K/Akt signaling pathway.
- This repression by miR-126 accelerates endothelial cell apoptosis, contributing to ASO progression.
- Targeting miR-126 may offer a therapeutic strategy for ASO.
Related Concept Videos
PI3K/mTOR/AKT Signaling Pathway
Apoptosis
The Eukaryotic Promoter Region
The Eukaryotic Promoter Region
Arteries of Lower Limbs
Veins of Lower Limbs
Formed by the union of the medial and lateral plantar veins, the posterior tibial vein, rising through the calf muscle, assimilates the fibular vein. The anterior tibial vein, a superior extension of the foot's dorsalis pedis vein, merges with the posterior tibial vein at the...

