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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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CD36-mediated podocyte lipotoxicity promotes foot process effacement.

Wei Hua¹, Lan Peng², Xue-Mei Chen³

¹Department of Nephrology, The First Affiliated Hospital of Chongqing Medical and Pharmaceutical College, Chongqing 400000, China.

Open Medicine (Warsaw, Poland)

|April 8, 2024

Summary

CD36 promotes fatty acid-induced podocyte damage and kidney injury through oxidative stress. Inhibiting CD36 may offer early treatment for lipotoxicity-related renal dysfunction.

Keywords:

CD36 ROS foot process effacement palmitic acid podocyte

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Area of Science:

Nephrology
Metabolic Disorders
Cell Biology

Background:

Lipid metabolism disorders cause lipotoxicity, leading to renal injury.
Hyperlipidemia-induced kidney injury primarily damages podocytes.
CD36 facilitates fatty acid uptake, causing toxic lipid accumulation and podocyte lipotoxicity.

Purpose of the Study:

To investigate the role of CD36 in fatty acid-induced podocyte damage.
To explore the potential of CD36 inhibition for treating early-stage kidney injury.

Main Methods:

Rats were fed a high-fat diet (HFD) or a normal diet.
Podocytes were treated with palmitic acid (PA) and CD36 inhibitor sulfo-N-succinimidyl oleate (SSO).
Protein expression, fatty acid accumulation, and ROS production were analyzed.

Main Results:

HFD-fed rats exhibited podocyte foot process effacement and proteinuria.
CD36 expression increased in HFD rats and PA-treated podocytes.
SSO treatment reduced lipid accumulation, ROS production, and cytoskeleton damage in podocytes.

Conclusions:

CD36 mediates fatty acid-induced podocyte damage via oxidative stress.
CD36 inhibitors show promise for the early treatment of kidney injury.