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Updated: Jan 26, 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
c-Src is in the effector pathway linking uPAR and podocyte injury
Urokinase-type plasminogen activator receptor (uPAR) plays a role in kidney disease. Targeting uPAR may offer new treatment strategies for focal segmental glomerulosclerosis (FSGS).
Area of Science:
- Nephrology
- Molecular Biology
- Immunology
Background:
- The urokinase-type plasminogen activator receptor (uPAR) is implicated in kidney physiology and pathology.
- uPAR regulates plasmin generation and functions within the innate immune system.
Purpose of the Study:
- To investigate the role of uPAR in podocyte injury and focal segmental glomerulosclerosis (FSGS).
Main Methods:
- Generation of transgenic mice expressing Plaur RNA in glomerular podocytes.
- Assessment of podocyte injury markers, including c-Src phosphorylation and proteinuria.
- Evaluation of Plaur-transgenic mice on a β3 integrin-deficient background.
- Analysis of renal biopsies from FSGS patients and other glomerular diseases.
Main Results:
- Transgenic mice expressing Plaur in podocytes exhibited podocyte injury, proteinuria, and FSGS.
- Protection from podocyte injury was observed in Plaur-transgenic mice on a β3 integrin-deficient background.
- Increased c-Src phosphorylation in podocytes was detected in FSGS patient biopsies, but not in other glomerular diseases.
Conclusions:
- Findings suggest a novel mechanism of podocyte injury in FSGS involving uPAR.
- Targeting uPAR may represent a potential therapeutic strategy for FSGS.
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