ArticleImmunity, inflammation and disease2023
KDM2B regulates inflammation and oxidative stress of sepsis via targeting NF-κB and AP-1 pathways.
Article in Immunity, inflammation and disease, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- Transcriptome and weighted gene co-expression network analysis identify hub genes and pathways in rat kidneys after deep hypothermic circulatory arrest.Renal failure · 2026Article
- KDM2B controls HIF levels and activity through its JmjC and CxxC domains.The Biochemical journal · 2026Article
- Serum HDAC3 as an early biomarker for prediction and staging of sepsis-associated AKI: prospective cohort study.BMC infectious diseases · 2026Article
- Mitochondrial dysfunction in sepsis-induced immunoparalysis: from immune-cell metabolic reprogramming to clinical biomarkers.Frontiers in immunology · 2026Review
- Histone demethylase inhibitors: developmental insights and current status.Future medicinal chemistry · 2025Review
- Network expression analysis identifies and experimentally validates the involvement of Fosb in acute kidney injury.FASEB bioAdvances · 2025Article
- CircMAPK1 induces cell pyroptosis in sepsis-induced lung injury by mediating KDM2B mRNA decay to epigenetically regulate WNK1.Molecular medicine (Cambridge, Mass.) · 2024Article
- From immune dysregulation to organ dysfunction: understanding the enigma of Sepsis.Frontiers in microbiology · 2024Review
- KDM2B regulates inflammation and oxidative stress of sepsis via targeting NF-κB and AP-1 pathways.Immunity, inflammation and disease · 2023Article
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3 authors.
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Abstract
backgroundsThe kidney is an easily affected organ with sepsis which is a main underlying cause of acute kidney injury (AKI). Histone-modifying lysine-specific demethylase 2B (KDM2B) is involved in numerous pathological processes, such as cell senescence and tumor development. However, the role of KDM2B in sepsis-induced AKI is unclear. OBJECTS: To investigate the role of KDM2B on cell viability, inflammation and oxidative stress of sepsis-associated AKI, and the involved signaling pathways.
methodsAn AKI model in vitro was established through lipopolysaccharide (LPS)-induction in HK-2 cells. Western blots were performed to evaluate the expression of KDM2B, cyclooxygenase 2 (COX2), inducible nitric oxide synthase (iNOS), p65, c-Jun and c-Fos, as well as p65 phosphorylation. Cell viability was measured using CCK-8 kit. ELISA was performed to analyze the production of layered double hydroxide (LDH), tumor necrosis factor (TNF)-α, interleukin (IL)-1β, IL-18, vascular cell adhesion molecule-1 (VCAM-1), superoxide dismutase (SOD), malondialdehyde (MDA), glutathione (GSH), and H
resultsKDM2B knockdown alleviated LPS-induced cytotoxicity, decreased LDH release, and improved cell viability. KDM2B knockdown reduced concentration of inflammation-related molecules including TNF-α, IL-1β, IL-18, and VCAM-1, and inhibited their transcription. Moreover, KDM2B knockdown promoted the quantity of SOD and GSH, while declined the production of MDA, H
conclusionKDM2B knockdown reduced cytotoxicity, inflammation and oxidative stress in LPS-induced AKI via inhibiting NF-κB and AP-1 pathways, indicating KDM2B may be a promising therapeutic target for the treatment of sepsis-associated AKI.
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