ArticleMediators of inflammation2021
Release of HMGB1 in Podocytes Exacerbates Lipopolysaccharide-Induced Acute Kidney Injury.
Article in Mediators of inflammation, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 19 citations in OpenAlex.
- Immunological mechanisms and novel therapeutic strategies for sepsis‑associated acute kidney injury (Review).International journal of molecular medicine · 2026Review
- Immune podocyte injury in autoimmune glomerular diseases.Frontiers in immunology · 2026Review
- Crosstalk of regulated cell death pathways in sepsis-associated acute kidney injury: implications for therapy.Frontiers in cell and developmental biology · 2026Review
- The role of mitochondrial reactive oxygen species in initiating mitochondrial damage and inflammation in wasp-venom-induced acute kidney injury.Journal of toxicologic pathology · 2025Article
- High-mobility group box 1 in acute kidney injury.Frontiers in pharmacology · 2025Review
- Review
- HMGB1 lactylation drives neutrophil extracellular trap formation in lactate-induced acute kidney injury.Frontiers in immunology · 2024Article
- STING deficiency protects against wasp venom-induced acute kidney injury.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2023Article
- Understanding the podocyte immune responses in proteinuric kidney diseases: from pathogenesis to therapy.Frontiers in immunology · 2023Review
- Targeting HMGB1: A Potential Therapeutic Strategy for Chronic Kidney Disease.International journal of biological sciences · 2023Review
- HMGB1 is a critical molecule in the pathogenesis of Gram-negative sepsis.Journal of intensive medicine · 2022Review
- Determination of HMGB1 in hepatitis B virus-related acute-on-chronic liver failure patients with acute kidney injury: Early prediction and prognostic implications.Frontiers in pharmacology · 2022Article
- The Intersection of Acute Kidney Injury and Non-Coding RNAs: Inflammation.Frontiers in physiology · 2022Review
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveAcute kidney injury (AKI) usually occurs during sepsis. Inflammation factors, such as high-mobility group box 1 (HMGB1), are dramatically upregulated under septic conditions. In our current work, the functions of HMGB1 in AKI were explored.
methodsAn AKI model was induced by the lipopolysaccharide (LPS) challenge in C57 mice. Podocytes were challenged by LPS for different durations. Subsequently, podocytes transfected with HMGB1 siRNA were exposed to LPS for 24 h. The expressions of supernatant HMGB1 and cellular active caspase-3 were examined by Western blotting analysis. To explore the effect of HMGB1 on tubular epithelial cells (TECs), HK-2 cells were exposed to HMGB1 at various concentrations for 24 h. Epithelial-mesenchymal transition (EMT) of HK-2 cells was evaluated by Western blotting analysis. Mitochondrial division and apoptosis of HK-2 cells were assessed by MitoTracker Red and Western blotting analysis, respectively.
resultsCompared with the sham control group, the expression of HMGB1 was increased in the kidney of AKI mice. Moreover, the expression of supernatant HMGB1 was increased in LPS-challenged podocytes compared with the control group. Knockdown of HMGB1 attenuated LPS-induced podocyte injury. Besides, EMT in TECs was triggered by HMGB1. Mitochondrial damage and apoptosis of HK-2 cells exposed to HMGB1 were markedly elevated compared with the control group.
conclusionsCollectively, HMGB1 release in podocytes was induced by LPS, subsequently leading to exacerbated AKI.
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