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Updated: Oct 19, 2025

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
Formyl peptide receptor 1 promotes podocyte injury through regulation of mitogen-activated protein kinase pathways
Jun Zhang1, Ting Ding1, Dongxing Tang1
1The Second Affiliated Hospital, Department of Nephropathy and Rheumatism, Hunan Province End Stage Renal Disease Clinical Medical Research Center, Hengyang Medical school, University of South China, Hengyang hunan 421001, China.
Abstract:
Podocyte injury contributes to glomerular injury and is implicated in the pathogenesis of diabetic nephropathy. Formyl peptide receptor (FPR) 1 is abundantly expressed in neutrophils and mediates intracellular transport of Ca 2+. Intracellular Ca 2+ regulates pathological process in renal podocyte and plays a role in diabetic nephropathy. However, the role of formyl peptide receptor 1 in podocyte injury of diabetic nephropathy has not been reported yet. Firstly, a rat model with diabetic nephropathy was established by streptozotocin injection, and a cell model was established via high glucose treatment of mouse podocytes (MPC5). Formyl peptide receptor 1 was enhanced in streptozotocin-induced rats and high glucose-treated MPC5. Secondly, streptozotocin injection promoted the glomerular injury with decreased nephrin and podocin. However, tail injection with adenovirus containing shRNA for silencing of formyl peptide receptor 1 attenuated streptozotocin-induced glomerular injury and the decrease in nephrin and podocin. Moreover, silencing of formyl peptide receptor 1 repressed cell apoptosis of podocytes in diabetic rats and high glucose-treated MPC5. Lastly, protein expression levels of p-p38, p-ERK, and p-JNK protein were up-regulated in streptozotocin-induced rats and high glucose-treated MPC5. Silencing of formyl peptide receptor 1 attenuated high glucose-induced increase in p-p38, p-ERK, and p-JNK in MPC5, and over-expression of formyl peptide receptor 1 aggravated high glucose-induced increase in p-p38, p-ERK, and p-JNK. In conclusion, inhibition of formyl peptide receptor 1 preserved glomerular function and protected against podocyte dysfunction in diabetic nephropathy.
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