ArticleJournal of bioenergetics and biomembranes2023
Toll-like receptor 4 promotes the inflammatory response in septic acute kidney injury by promoting p38 mitogen-activated protein kinase phosphorylation.
Article in Journal of bioenergetics and biomembranes, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 20 citations in OpenAlex.
- Downregulation of AQP9 Ameliorates NLRP3 Inflammasome-Dependent Inflammation and Pyroptosis in Crohn's Disease by Inhibiting the p38 MAPK Signaling Pathway.Molecular biotechnology · 2026Article
- Pioglitazone Attenuates Sepsis-Associated Acute Kidney Injury by Modulating TLR-4/NF-κB Signaling and Improving Survival and Renal Function.Journal of clinical medicine · 2026Article
- Ergosterol alleviates lipopolysaccharide-induced acute kidney injury in rats via a mechanistic modulation of TLR4/p-p38/NF-κB, iNOS/NO and Nrf2/HO-1 signaling pathways.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Integration of RNA-seq and scRNA-seq to investigate the role of cell cycle-related biomarkers in sepsis.PloS one · 2026Article
- Protective effect of Lonicerae Japonicae Flos extract against doxorubicin-induced myocardial injury in mice and the possible mechanisms.Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2025Article
- Beyond the bladder: Escherichia coli UTIs drive systemic inflammation and RANKL-mediated bone resorption.Irish journal of medical science · 2025Article
- Gum Acacia-Dexamethasone Combination Attenuates Sepsis-Induced Acute Kidney Injury in Rats via Targeting SIRT1-HMGB1 Signaling Pathway and Preserving Mitochondrial Integrity.Pharmaceuticals (Basel, Switzerland) · 2025Article
- Programmed cell death regulates hematopoietic cell homeostasis under radiation conditions.Stem cell research & therapy · 2025Article
- Targeting glial fibrillary acidic protein in glaucoma: a monoclonal antibody approach to modulate glial reactivity and neuroinflammation for neuroprotection.Journal of neuroinflammation · 2025Article
- Molecular mechanisms and therapeutic interventions in acute kidney injury: a literature review.BMC nephrology · 2025Review
- Post-translational modifications in sepsis-induced acute kidney injury: mechanisms and perspectives.Frontiers in pharmacology · 2025Review
- Cytokines in sepsis: a critical review of the literature on systemic inflammation and multiple organ dysfunction.Frontiers in immunology · 2025Review
- Chinese medicine in the treatment of chronic hepatitis B: The mechanisms of signal pathway regulation.Heliyon · 2024Review
- Construction of a Multi-Indicator Model for Abscess Prediction in Granulomatous Lobular Mastitis Using Inflammatory Indicators.Journal of inflammation research · 2024Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Septic acute kidney injury (AKI) contributes to the mortality and morbidity of sepsis patients. Toll-like Receptor 4 (TLR4) has prominent roles in septic AKI. This study investigated the functions of TLR4 in septic AKI. A septic AKI mouse model was established by cecal ligation and puncture surgery. Mouse kidney function and kidney tissue lesion were examined using corresponding kits and H&E staining. The in vitro cell model of septic AKI was established by lipopolysaccharide induction. Cell viability, inflammatory factor (TNF-α, IL-6, IL-4, IL-1β, IL-18) levels, pyroptotic cell number changes, lactate dehydrogenase (LDH) activity, myeloperoxidase (MOP) concentration, and levels of pyroptosis-associated protein and MyD88, TRIF and p38 MAPK phosphorylation were determined by MTT, ELISA, FAM-FLICA Caspase-1 Detection kit, other corresponding kits, and Western blot. TLR4 was highly expressed in septic AKI mouse kidney tissues and human septic AKI cells. TLR4 knockdown alleviated kidney injury, increased cell viability, and reduced LDH activity and MPO concentration. TLR4 knockdown reduced cell pyroptosis by repressing p38 MAPK phosphorylation through MyD88/TRIF, suppressed pro-inflammatory factor (TNF-α, IL-6, IL-4, IL-1β, IL-18) levels, promoted anti-inflammatory factor (IL-4) level, and reduced inflammatory response, thus playing a protective role in septic AKI. Briefly, TLR4 promoted the inflammatory response in septic AKI by promoting p38 MAPK phosphorylation through MyD88/TRIF.
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