ArticleJournal of cellular and molecular medicine2020
LIGHT aggravates sepsis-associated acute kidney injury via TLR4-MyD88-NF-κB pathway.
Article in Journal of cellular and molecular medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 46 citations in OpenAlex.
- Engineered hollow Prussian blue nanoparticles for synergistic anti-inflammatory therapy in sepsis.Materials today. Bio · 2026Article
- MiR-146b-5p/ERBB4 Axis Drives LPS-induced Acute Kidney Injury by Modulating NF-κB/p65.Biochemical genetics · 2026Article
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- Integration of intragraft transcriptomics and urinary cytokines identifies CXCL10 and FasL signature in subclinical acute rejection.Scientific reports · 2026Article
- Current Status and Future Prospects of Research on Sepsis-Related Acute Kidney Injury.International journal of molecular sciences · 2026Review
- Xuebijing injection alleviates septic acute kidney injury by modulating inflammation, mitochondrial dysfunction, and endoplasmic reticulum stress.Renal failure · 2025Article
- TNFSF14-HVEM/LTβR Exacerbates Keratinocyte Abnormalities and IMQ-Induced Psoriatic Skin Inflammation via Activating NF-κB/TWIST1 Signalling Pathway.Journal of cellular and molecular medicine · 2025Article
- The gut-kidney axis in urolithiasis: roles of gut microbiota, metabolites, and therapeutic implications.Frontiers in microbiology · 2025Review
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- Protective effect of modified Huangqi Chifeng decoction on immunoglobulin A nephropathy through toll-like receptor 4/myeloid differentiation factor 88/nuclear factor-kappa B signaling pathway.Journal of traditional Chinese medicine = Chung i tsa chih ying wen pan · 2024Article
- Trichinella spiralis galectin binding to toll-like receptor 4 induces intestinal inflammation and mediates larval invasion of gut mucosa.Veterinary research · 2023Article
- Toll-like receptor 4 promotes the inflammatory response in septic acute kidney injury by promoting p38 mitogen-activated protein kinase phosphorylation.Journal of bioenergetics and biomembranes · 2023Article
- Blockade of Indoleamine 2,3-Dioxygenase attenuates lipopolysaccharide-induced kidney injury by inhibiting TLR4/NF-κB signaling.Clinical and experimental nephrology · 2023Article
- Platelet-derived extracellular vesicles aggravate septic acute kidney injury via delivering ARF6.International journal of biological sciences · 2023Article
- LIGHT Amplification by NF-Mediators of inflammation · 2023Article
- NETosis: an emerging therapeutic target in renal diseases.Frontiers in immunology · 2023Review
- LIGHT deficiency attenuates acute kidney disease development in an in vivo experimental renal ischemia and reperfusion injury model.Cell death discovery · 2022Article
- Neutrophil membrane-coated therapeutic liposomes for targeted treatment in acute lung injury.International journal of pharmaceutics · 2022Article
- Therapeutic Potential of Allicin and Aged Garlic Extract in Alzheimer's Disease.International journal of molecular sciences · 2022Review
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Sepsis-associated acute kidney injury (SA-AKI) is a common clinical critical care syndrome. It has received increasing attention due to its high morbidity and mortality; however, its pathophysiological mechanisms remain elusive. LIGHT, the 14th member of the tumour necrosis factor (TNF) superfamily and a bidirectional immunoregulatory molecule that regulates inflammation, plays a pivotal role in disease pathogenesis. In this study, mice with an intraperitoneal injection of LPS and HK-2 cells challenged with LPS were employed as a model of SA-AKI in vivo and in vitro, respectively. LIGHT deficiency notably attenuated kidney injury in pathological damage and renal function and markedly mitigated the inflammatory reaction by decreasing inflammatory mediator production and inflammatory cell infiltration in vivo. The TLR4-Myd88-NF-κB signalling pathway in the kidney of LIGHT knockout mice was dramatically down-regulated compared to the controls. Recombinant human LIGHT aggravated LPS-treated HK-2 cell injury by up-regulating the expression of the TLR4-Myd88-NF-κB signalling pathway and inflammation levels. TAK 242 (a selective TLR4 inhibitor) reduced this trend to some extent. In addition, blocking LIGHT with soluble receptor fusion proteins HVEM-Fc or LTβR-Fc in mice attenuated renal dysfunction and pathological damage in SA-AKI. Our findings indicate that LIGHT aggravates inflammation and promotes kidney damage in LPS-induced SA-AKI via the TLR4-Myd88-NF-κB signalling pathway, which provide potential strategies for the treatment of SA-AKI.
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