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VEGF ameliorates acute kidney injury by suppressing ferroptosis through activation of the ERK1/2-NRF2 pathway
Journal article   Peer reviewed

VEGF ameliorates acute kidney injury by suppressing ferroptosis through activation of the ERK1/2-NRF2 pathway

Xiangtian Liu, Yuqi Song, Weikun Tian, Liping Ye, Dongxiao Li, Meifeng Li, Xinghan Tian and Xiaoli Li
Growth factors (Chur, Switzerland), Vol.43(3), pp.155-165
03/07/2025
DOI: https://doi.org/10.1080/08977194.2025.2533773
PMID: 40694052

Abstract

Acute Kidney Injury - drug therapy Acute Kidney Injury - metabolism Acute Kidney Injury - pathology Amino Acid Transport System y Animals Cell Line Disease Models, Animal Ferroptosis - drug effects Glutathione - metabolism Humans Male Malondialdehyde - metabolism MAP Kinase Signaling System - drug effects Mice Mice, Inbred C57BL NF-E2-Related Factor 2 - metabolism Oxidative Stress - drug effects Phospholipid Hydroperoxide Glutathione Peroxidase - metabolism Reactive Oxygen Species - metabolism Vascular Endothelial Growth Factor A - metabolism Vascular Endothelial Growth Factor A - pharmacology
Vascular endothelial growth factor (VEGF) plays a crucial role in maintaining renal homeostasis. However, the precise impact of VEGF on ferroptosis in acute kidney injury (AKI) remains incompletely understood. This study aims to investigate the effects of VEGF on ferroptosis in the model of AKI and to elucidate the underlying mechanisms. We used C57BL mice and HK-2 cells to construct sepsis-associated AKI models. We assessed renal function, cell viability, and tissue levels of iron, malondialdehyde (MDA), and glutathione (GSH) in mice. Intracellular reactive oxygen species (ROS), mitochondrial membrane potential, and electron microscopy-detected cellular changes were also measured. Western blotting analyzed key ferroptosis-related proteins (SLC7A11, GPX4) and components of the ERK1/2-NRF2-GPX4 pathway. VEGF treatment significantly reduced oxidative stress by lowering ROS and MDA levels while increasing GSH. Additionally, VEGF165 activated the ERK1/2-NRF2 pathway, mitigating ferroptosis.

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