ArticleCell communication and signaling : CCS2024
Endothelial CXCR2 deficiency attenuates renal inflammation and glycocalyx shedding through NF-κB signaling in diabetic kidney disease.
Article in Cell communication and signaling : CCS, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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16 citing papers in PubMed, 14 citations in OpenAlex.
- Molecular mechanisms and novel therapeutic targets of diabetic kidney disease.Chinese medical journal · 2026Review
- TRIM38 alleviates the pathogenesis of diabetic nephropathy by suppressing NF-κB activation via inducing RIPK1 degradation.Journal of physiology and biochemistry · 2026Article
- Glycocalyx degradation: exploring related mechanisms, pathophysiological significance, and therapeutic prospects.Journal of physiology and biochemistry · 2026Review
- Gene modification: Exploring the potential in treating kidney diseases.Pharmacological research · 2026Review
- Porphyromonas gingivalis-derived outer membrane vesicles promote vascular endothelial glycocalyx injury via the PPAD/CitH3/B3GAT1 pathway.Journal of nanobiotechnology · 2026Article
- From a Shared Stress to Cell-Type-Specific Responses: The Heterogeneous Mechanisms of High Glucose-Induced Cellular Senescence in Diabetic Kidney Disease.Journal of diabetes research · 2026Review
- Deconvolution of molecular mechanisms in di-n-butyl phthalate/mono-n-butyl phthalate induced diabetic kidney disease by integrated machine learning and molecular docking.BMC nephrology · 2025Article
- NF-κB p65 mediated lnc-Traf3ip2 exacerbates renal fibrosis in diabetic kidney disease.Acta diabetologica · 2025Article
- Correlation analysis between hemoglobin and type 2 diabetic nephropathy: a two-center retrospective study.Acta diabetologica · 2025Article
- The glycocalyx: a key target for treatment of severe acute pancreatitis-associated multiple organ dysfunction syndrome.Human cell · 2025Review
- Therapeutic potential of naturally derived carbon dots in sepsis-associated acute kidney injury.Chinese medicine · 2025Article
- Total flavonoids fromFrontiers in medicine · 2025Article
- Immunological profiling in type 2 diabetes mellitus and type 2 diabetic kidney disease: insights from single-cell LacNAc sequencing.Frontiers in endocrinology · 2025Article
- Investigating the metabolic reprogramming mechanisms in diabetic nephropathy: a comprehensive analysis using bioinformatics and machine learning.Frontiers in cell and developmental biology · 2025Article
- Immune Cell Migration to Cancer.Cells · 2024Review
- Pretreatment with Indole-3-Propionic Acid Attenuates Lipopolysaccharide-Induced Cardiac Dysfunction and Inflammation Through the AhR/NF-κB/NLRP3 Pathway.Journal of inflammation research · 2024Article
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe incidence of diabetic kidney disease (DKD) continues to rapidly increase, with limited available treatment options. One of the hallmarks of DKD is persistent inflammation, but the underlying molecular mechanisms of early diabetic kidney injury remain poorly understood. C-X-C chemokine receptor 2 (CXCR2), plays an important role in the progression of inflammation-related vascular diseases and may bridge between glomerular endothelium and persistent inflammation in DKD.
methodsMultiple methods were employed to assess the expression levels of CXCR2 and its ligands, as well as renal inflammatory response and endothelial glycocalyx shedding in patients with DKD. The effects of CXCR2 on glycocalyx shedding, and persistent renal inflammation was examined in a type 2 diabetic mouse model with Cxcr2 knockout specifically in endothelial cells (DKD-Cxcr2
resultsCXCR2 was associated with early renal decline in DKD patients, and endothelial-specific knockout of CXCR2 significantly improved renal function in DKD mice, reduced inflammatory cell infiltration, and simultaneously decreased the expression of proinflammatory factors and chemokines in renal tissue. In DKD conditions, glycocalyx shedding was suppressed in endothelial Cxcr2 knockout mice compared to Cxcr2
conclusionsTaken together, under DKD conditions, activation of CXCR2 exacerbates inflammation through regulation of the NF-κB pathway, leading to endothelial glycocalyx shedding and deteriorating renal function. Endothelial CXCR2 deficiency has a protective role in inflammation and glycocalyx dysfunction, suggesting its potential as a promising therapeutic target for DKD treatment.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.