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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
Acetate ameliorates membranous nephropathy by modulating the immune response and podocyte function.
Jing Liu1,2,3,4,5,6, Yan-Yan Cui5, Kai Zheng7
1Renal Division, Peking University First Hospital, Beijing, 100034, China.
BMC Nephrology
|July 6, 2026
Summary
Acetate, a short-chain fatty acid (SCFA), reduces proteinuria in experimental membranous nephropathy (MN) by modulating immune responses and protecting podocytes. This suggests targeting acetate pathways may be a safe adjunctive therapy for MN.
Area of Science:
- Nephrology
- Immunology
- Metabolomics
Background:
- Membranous nephropathy (MN) is an antibody-mediated podocytopathy causing proteinuria via immune deposits and complement activation.
- Short-chain fatty acids (SCFAs) have immunomodulatory roles, but their therapeutic potential in MN is unclear.
Purpose of the Study:
- To investigate the therapeutic effects and mechanisms of SCFAs, specifically acetate, propionate, and butyrate, in a rat model of membranous nephropathy.
Main Methods:
- Evaluated acetate, propionate, and butyrate in a passive Heymann nephritis (PHN) rat model.
- Assessed proteinuria, glomerular injury, immune deposits, and podocyte markers.
- Analyzed splenic T-cell subsets and in vitro podocyte responses to MN plasma with/without acetate.
Main Results:
- SCFAs reduced proteinuria and ameliorated glomerular/ultrastructural injury in PHN rats.
- Acetate decreased immune deposits, modulated T-cell responses (increased Tregs), and protected podocytes.
- Acetate's effects involved GPR43, reduced HDAC activity, and improved podocyte function in vitro.
Conclusions:
- Acetate ameliorates experimental MN through immunomodulation and podocyte protection.
- Targeting acetate pathways represents a promising, low-toxicity adjunctive strategy for MN treatment.
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