ArticleInflammation2019
Fractalkine is Involved in Lipopolysaccharide-Induced Podocyte Injury through the Wnt/β-Catenin Pathway in an Acute Kidney Injury Mouse Model.
Article in Inflammation, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 32 citations in OpenAlex.
- CX3CL1 deficiency ameliorates acute kidney injury by inhibiting macrophage mitochondrial dysfunction and mtDNA-cGAS-STING signaling.Cell death discovery · 2025Article
- The mechanism of enterogenous toxin methylmalonic acid aggravating calcium-phosphorus metabolic disorder in uremic rats by regulating the Wnt/β-catenin pathway.Molecular medicine (Cambridge, Mass.) · 2025Article
- Obtusifolin inhibits podocyte apoptosis by inactivating NF-κB signaling in acute kidney injury.Cytotechnology · 2024Article
- Early diagnostic biomarkers for acute kidney injury using cisplatin-induced nephrotoxicity in rat model.Current research in toxicology · 2023Article
- Podocyte specific deletion of PKM2 ameliorates LPS-induced podocyte injury through beta-catenin.Cell communication and signaling : CCS · 2022Article
- Lipopolysaccharide-induced podocyte injury is regulated by calcineurin/NFAT and TLR4/MyD88/NF-κB signaling pathways through angiopoietin-like protein 4.Genes & diseases · 2022Article
- Tacrolimus alleviates LPS-induced AKI by inhibiting TLR4/MyD88/NF-κB signalling in mice.Journal of cellular and molecular medicine · 2022Article
- Downregulation of miR-29b-3p aggravates podocyte injury by targeting HDAC4 in LPS-induced acute kidney injury.The Kaohsiung journal of medical sciences · 2021Article
- Review on Inflammation Markers in Chronic Kidney Disease.Biomedicines · 2021Review
- Release of HMGB1 in Podocytes Exacerbates Lipopolysaccharide-Induced Acute Kidney Injury.Mediators of inflammation · 2021Article
- The kidney, COVID-19, and the chemokine network: an intriguing trio.International urology and nephrology · 2021Review
- Low-Dose Aspirin Prevents Kidney Damage in LPS-Induced Preeclampsia by Inhibiting the WNT5A and NF-κB Signaling Pathways.Frontiers in endocrinology · 2021Article
- The Active Compounds and Therapeutic Target ofFrontiers in medicine · 2021Review
- [Fractalkine inhibits lipopolysaccharide-induced M1 polarization of macrophages by activating Wnt/β-catenin signaling pathway].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2020Article
- Phillyrin Relieves Lipopolysaccharide-Induced AKI by Protecting Against Glycocalyx Damage and Inhibiting Inflammatory Responses.Inflammation · 2020Article
- Fractalkine mediates lymphocyte inflammation and tubulointerstitial lesions by modifying the Treg/Th17 balance in lupus-prone MRL/lpr mice.American journal of translational research · 2020Article
- FKN Facilitates HK-2 Cell EMT and Tubulointerstitial Lesions via the Wnt/β-Catenin Pathway in a Murine Model of Lupus Nephritis.Frontiers in immunology · 2019Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Injury to podocytes leads to proteinuria, a hallmark of most glomerular diseases as well as being associated with the progression of kidney disease. Activation of the Wnt/β-catenin pathway is associated with the pathogenesis of podocyte dysfunction and can play a role in renal injury. Furthermore, the expression of fractalkine (FKN) induced by lipopolysaccharides (LPS) is also one of crucial inflammation factors closely related to renal tissue damage. The aim of this study is to explore the mechanism of LPS-induced FKN expression leading to podocyte injury and contribute to acute kidney injury (AKI) through regulation of Wnt/β-catenin pathway. An AKI model was established for in vivo experiments and blood was collected for serum BUN and Cr measurement, and histopathological features of the kidneys were studied by PASM and IHC staining. For in vitro experiments, a mouse podocyte cell line was stimulated with different concentrations of LPS for 24 and 48 h after which podocyte viability and apoptosis of cells were evaluated. The expression of podocyte-specific markers, FKN and Wnt/β-catenin pathway mRNA and protein was detected in mice and cells by using qRT-PCR and western blotting. LPS induced the expression of FKN and activation of the Wnt/β-catenin pathway, leading to a decrease of podocyte-specific proteins which resulted in poor renal pathology and dysfunction in the AKI mouse model. Moreover, LPS treatment significantly decreased cell viability and induced podocyte apoptosis in a dose-dependent manner that causes changes in the expression of podocyte-specific proteins through activation of FKN and the Wnt/β-catenin pathway. Thus, the expression of FKN and Wnt/β-catenin pathway by LPS is closely associated with podocyte damage or loss and could therefore account for progressive AKI. Our findings indicate that LPS induce podocyte injury and contribute to the pathogenesis of AKI by upregulating the expression of FKN and Wnt/β-catenin pathway.
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