CircRNA_1156 Attenuates Neodymium Nitrate-Induced Hepatocyte Ferroptosis by Inhibiting the ACSL4/PKCβII Signaling Pathway

CircRNA_1156 Attenuates Neodymium Nitrate-Induced Hepatocyte Ferroptosis by Inhibiting the ACSL4/PKCβII Signaling Pathway

Ferroptosis, a form of regulated cell death driven by lipid peroxidation, has been implicated in the pathogenesis of liver diseases. This study investigates the role of circRNA_1156 in neodymium nitrate (Nd(NO<sub>3</sub>)<sub>3</sub>)-induced hepatocyte ferroptosis. Our in v...

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Main Authors: Ning Wang, Jing Leng, Jing Xu, Kelei Qian, Zhiqing Zheng, Gonghua Tao, Ping Xiao, Xinyu Hong
Format: Article
Language:English
Published: MDPI AG 2025-06-01
Series:Antioxidants
Subjects:
circRNA_1156
neodymium nitrate
ferroptosis
ACSL4/PKCβII pathway
hepatocyte injury
Online Access:https://www.mdpi.com/2076-3921/14/6/700
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Summary:Ferroptosis, a form of regulated cell death driven by lipid peroxidation, has been implicated in the pathogenesis of liver diseases. This study investigates the role of circRNA_1156 in neodymium nitrate (Nd(NO<sub>3</sub>)<sub>3</sub>)-induced hepatocyte ferroptosis. Our in vitro experiments revealed that exposure to Nd(NO<sub>3</sub>)<sub>3</sub> (1.2 µM) significantly reduced the viability of AML12 hepatocytes (<i>p</i> < 0.01), increased levels of reactive oxygen species (ROS) and malondialdehyde (MDA) (<i>p</i> < 0.001), and depleted glutathione (GSH) (<i>p</i> < 0.001). However, overexpression of circRNA_1156 effectively reversed these effects and suppressed the expression of ACSL4 and PKCβII (<i>p</i> < 0.01). In our in vivo experiments, chronic exposure to Nd(NO<sub>3</sub>)<sub>3</sub> (7–55 mg/kg for 180 days) induced hepatic iron deposition, mitochondrial damage, and activation of the ACSL4/PKCβII pathway (<i>p</i> < 0.01). These adverse effects were significantly ameliorated by circRNA_1156 overexpression (<i>p</i> < 0.05). Our findings identify circRNA_1156 as a novel inhibitor of Nd(NO<sub>3</sub>)<sub>3</sub>-induced ferroptosis via downregulation of the ACSL4/PKCβII pathway, providing valuable therapeutic insights for hepatotoxicity caused by rare earth element compounds.
ISSN:2076-3921

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