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Mechanism of Kemeng Fang's Inhibition of Podocyte Apoptosis in Rats with Membranous Nephropathy through the PI3K/AKT Signaling Pathway
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Genistein Mitigates High Glucose-induced Podocyte Injury by Modulating Autophagy via the mTOR Signal
Yu Shan1, Ying Cai2, Yuhang Lian3
1Department of Nephrology, Kidney Disease Medical Center, General Hospital, Tianjin Medical University, National Key Clinical Specialty, Tianjin Key Medical Discipline, Tianjin, China.
Current Pharmaceutical Design
|June 9, 2026
Summary
High glucose damages kidney podocytes by disrupting autophagy and mTOR signaling. Genistein treatment protected podocytes by restoring autophagy and improving cellular functions, suggesting a therapeutic potential for diabetic kidney disease.
Area of Science:
- Nephrology
- Cell Biology
- Molecular Biology
Background:
- High glucose (HG) induces podocyte injury, a key factor in diabetic nephropathy.
- Autophagy dysregulation is implicated in HG-induced podocyte damage.
Purpose of the Study:
- To investigate autophagy alterations in podocytes under HG conditions.
- To evaluate the protective effects of genistein on HG-induced podocyte injury.
Main Methods:
- Podocytes cultured under normal glucose (NG) or HG conditions, treated with genistein or rapamycin.
- Proteomic analysis, immunoblotting, immunofluorescence, and ultrastructural examination.
- Functional assays for cell adhesion, migration, and cytoskeletal organization.
Main Results:
- HG reduced podocyte viability, increased mTOR phosphorylation, and impaired autophagic-lysosomal function.
- Proteomics identified enrichment in lysosome-, autophagy-, and mTOR-related pathways.
- Genistein treatment attenuated HG-induced injury, reducing mTOR phosphorylation and restoring autophagic function.
Conclusions:
- HG-induced podocyte injury involves mTOR signaling, autophagy markers, and integrin β1 dysfunction.
- Genistein demonstrates protective effects by modulating these interconnected pathways.
- Genistein may offer a therapeutic strategy for diabetic kidney disease by restoring autophagy.
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