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RNF113A Protects Against Sepsis-Induced Myocardial Injury via Activation of the Keap1/Nrf2 Axis to Reduce Ferroptosis
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DOI：10.1002/jbt.70970.png)
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Abstract
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Sepsis-induced myocardial injury (SIM) is a common complication of sepsis that can cause high morbidity and mortality. However, the molecular mechanisms underlying SIM have still not been fully elucidated. Ferroptosis is a novel form of cell death associated with oxidative stress and is characterised by elevated iron levels. In the present study, mouse cardiomyocytes (H9c2 cells) and C57BL/6 mice were treated with lipopolysaccharide (LPS) to establish an in vitro and an in vivo model of SIM, respectively. RNF113A, a member of the RING finger protein (RNF) family with E3 ligase activity, was downregulated in H9c2 cells treated with LPS compared to untreated cells. Overexpression of RNF113A reduced LPS-induced cardiac injury and ferroptosis both in vitro and in vivo. Mechanistically, RNF113A directly targets Keap1 and promotes its ubiquitination and degradation. This results in the activation of Nrf2 signaling. Our findings suggest that RNF113A directly targets Keap1 to activate Nrf2 signalling, which plays an essential role in the pathogenesis of SIM.
Keywords:
ferroptosis
Keap1
Nrf2
RNF113A
sepsis-induced myocardial injury
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