ArticleBiology direct2026
SF1 regulates the transcription of FDX1 to promote cuproptosis in pediatric sepsis-related acute lung injury by interacting with cJUN.
Article in Biology direct, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundPediatric sepsis, a major cause of acute lung injury (ALI), involves a dysregulated host response. Cuproptosis is a novel copper-dependent cell death process regulated by Ferredoxin 1 (FDX1). However, its role in pediatric sepsis-associated ALI is unknown. This study investigated the upstream regulation mechanism of FDX1, and its role in pediatric sepsis-related ALI.
methodsPeripheral blood mononuclear cells (PBMCs) were collected from septic children and healthy controls. All enrolled pediatric subjects were divided into three groups: healthy control group (N = 40), sepsis without ALI group (N = 30), and sepsis with ALI group (N = 30). The clinical significance of FDX1, steroidogenic factor 1 (SF1), and Jun proto-oncogene (cJUN) was assessed by qRT-PCR. A septic ALI cell model was established using LPS-treated BEAS-2B cells. Functional assays (CCK-8, TUNEL, ELISA) assessed viability, apoptosis, and inflammation. An in vivo cecal ligation and puncture (CLP) model was employed to confirm the role of FDX1. Molecular mechanisms (transcriptional regulation, protein interaction) were examined via ChIP, dual-luciferase, and Co-IP.
resultsFDX1, SF1, and cJUN levels were significantly elevated in pediatric sepsis patients, especially in those complicated with ALI, and the three genes were positively correlated with each other. In vitro, LPS induced BEAS-2B cell injury, inflammation, and cuproptosis. FDX1 overexpression exacerbated these effects, while its knockdown exerted protective effects. Mechanistically, SF1 directly bound to the FDX1 promoter to activate its transcription. SF1 physically interacted with cJUN, and they synergistically enhanced FDX1 transcription. Knockdown of cJUN abolished SF1-mediated FDX1 upregulation and its pro-cuproptotic effects. In vivo experiments demonstrated that FDX1 knockdown attenuated CLP-induced lung injury, inflammation, and cuproptosis.
conclusionsSF1, cJUN, and FDX1 may be closely involved in pediatric sepsis-related ALI. The physical interaction between SF1 and cJUN potentially modulates FDX1 transcription, which may contribute to cuproptosis and pediatric sepsis-related ALI progression.
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