ArticleAmerican journal of translational research2026
Cinnamaldehyde attenuates LPS-induced acute kidney injury by inhibiting ferroptosis via the Gsk3β/Nrf2/Gpx4 pathway.
Article in American journal of translational research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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Who cites it
1 citing paper in PubMed.
- Targeting Ferroptosis in Sepsis: Therapeutic Potential and Mechanisms of Natural Products and Traditional Chinese Medicine.Journal of inflammation research · 2026Review
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6 authors.
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Abstract
objectivesSepsis-induced acute kidney injury (AKI) is a critical complication with limited treatment options. We investigated the protective effects of cinnamaldehyde (CA) on lipopolysaccharide (LPS)-induced AKI and elucidated underlying mechanisms focusing on ferroptosis and the glycogen synthase kinase 3 beta (GSK3β)/nuclear factor erythroid 2-related factor 2 (Nrf2)/glutathione peroxidase 4 (GPX4) pathway.
methodsNetwork pharmacology, molecular docking, and experimental validation were integrated. LPS-induced AKI models were established in C57BL/6 mice and human proximal tubular epithelial HK-2 (HK-2) cells. CA effects on renal function, histological injury, inflammation, and ferroptosis markers were evaluated. GSK3β involvement was tested via lentiviral overexpression. Protein and mRNA levels were measured by Western blotting, quantitative polymerase chain reaction (qPCR), enzyme-linked immunosorbent assay (ELISA), and immunofluorescence.
resultsCA improved renal function and reduced tubular injury and inflammation. CA suppressed ferroptosis, evidenced by decreased malondialdehyde (MDA), iron, and lipid peroxidation, and normalization of GPX4 and acyl-CoA synthetase long chain family member 4 (ACSL4) expression. Network pharmacology and docking identified GSK3β as a key CA target; lentiviral GSK3β overexpression abolished CA's renoprotective and anti-ferroptotic effects. Mechanistically, CA activated Nrf2 and increased GPX4 expression via inhibition of the GSK3β/Nrf2/Kelch-like ECH-associated protein 1 (KEAP1) pathway.
conclusionsCA protects against LPS-induced AKI by inhibiting ferroptosis through modulation of the GSK3β/Nrf2/GPX4 axis, highlighting CA as a potential ferroptosis-targeted therapeutic candidate for septic AKI.
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