Targeting ALOX5 ameliorates renal tubular injury in ischemia-reperfusion-induced acute kidney injury via inhibition of ferroptosis.

ABSTRACT: Ischemia-reperfusion injury (IRI)-induced acute kidney injury (AKI) could be potentially lethal in clinic. We found lipoxygenases-5 (ALOX5) was upregulated in renal tubular cells in IRI-induced AKI; however, its underlying mechanism is not clear. In this study, we explore the function of ALOX in IRI-induced AKI using human renal proximal tubular epithelial cells (HK-2) and C57BL/6 mice. Alox5 knock-out mouse is constructed. Products of polyunsaturated fatty acids metabolized by ALOX5 in the kidney tissue are measured by UHPLC-HRMS/MS platform. Ferroptosis is measured upon ALOX5 intervention and Benzbromarone (BBR) intervention. The results indicate that in IRI-induced AKI, ALOX5 is up-regulated in the renal tubular epithelial cells and exacerbates the accumulation of lipid peroxides, which

SUBMITTER: Huang L 

PROVIDER: S-EPMC12484620 | biostudies-literature | 2025 Sep

REPOSITORIES: biostudies-literature