The protective mechanism is primarily through the inhibition of ferroptosis along the GSK3β/Nrf2/GPX4 pathway.
Analysis highlights the potential for cinnamaldehyde as a targeted therapy for septic acute kidney injury.
Future clinical tests are needed to validate these findings and confirm efficacy beyond laboratory settings.
Abstract
CA 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.