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The following is a summary of “CIAPIN1 attenuates ferroptosis via regulating PI3K/AKT pathway in LPS-induced podocytes,” published in the April 2025 issue of BMC Nephrology by Zhang et al. 

Cytokine-induced apoptosis inhibitor 1 (CIAPIN1) is a key anti-apoptotic protein, yet its role in ferroptosis, particularly in LPS-induced podocytes, remains unclear. 

Researchers conducted a retrospective study to examine CIAPIN1’s effects on ferroptosis in lipopolysaccharide (LPS)-induced podocytes.  

They recruited 50 patients with sepsis (aged 56.63 ± 10.33) with acute kidney injury (AKI), 50 patients with sepsis without AKI, and 50 healthy controls. An in vitro model of LPS-induced MPC5 podocytes was established. RT-qPCR and Western blotting were used to evaluate mRNA and protein expression, respectively. 

The results showed that serum CIAPIN1 was downregulated in patients with septic AKI and LPS-induced podocytes. CIAPIN1 overexpression (OE-CIAPIN1) attenuated cell proliferation and apoptosis in LPS-induced podocytes. OE-CIAPIN1 increased p-PI3K (p85, Tyr458) and p-Akt (Ser473) levels, elevated synaptopodin mRNA, and reduced desmin mRNA expression in MPC5 cells. Treatment with the PI3K/Akt inhibitor LY294002 reversed these effects. OE-CIAPIN1 decreased MDA and Fe2⁺ concentrations, while LY294002 treatment increased them. Additionally, OE-CIAPIN1 elevated solute carrier family 7 member 11 (SLC7A11) and glutathione peroxidase 4 (GPX4) levels, which were reversed by LY294002. 

Investigators found that serum CIAPIN1 inhibited LPS-induced ferroptosis in podocytes by regulating the PI3K/AKT signaling pathway. 

Source: bmcnephrol.biomedcentral.com/articles/10.1186/s12882-025-04123-1