ArticleLaboratory animal research2024
Observation of neutrophil extracellular traps in the development of diabetic nephropathy using diabetic murine models.
Article in Laboratory animal research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- Article
- Stage-specific elevation of MPO and NE mRNA expression in diabetic kidney disease and their independent associations with albuminuria.Molecular biology reports · 2026Article
- Article
- Oyster hydrolysate attenuates osteoarthritis progression by modulating inflammatory signaling and extracellular matrix homeostasis.Nutrition research and practice · 2026Article
- Neutrophils and neutrophil extracellular traps in diabetes mellitus and its complications: Mechanisms and therapeutic implications.iScience · 2026Review
- Beyond hyperglycemia: histone modification-mediated epigenetic dysregulation in diabetic retinopathy and nephropathy.Diabetology & metabolic syndrome · 2026Review
- Inflammation and Diabetic Kidney Disease.International journal of molecular sciences · 2026Review
- Anemia in diabetes mellitus: Pathogenetic aspects and the value of early erythropoietin therapy.Metabolism open · 2025Review
- Neutrophils: emerging perspectives on the pathogenesis of oral mucosal diseases.Frontiers in cellular and infection microbiology · 2025Review
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Authors and funding
12 authors.
Funding
Abstract
backgroundDiabetic nephropathy (DN) is a progressive complication among patients with diabetes and the most common cause of end-stage kidney disease. Neutrophil extracellular traps (NETs) are known to play a role in kidney disease, thus this study aimed to determine their role in the development of diabetic kidney disease using diabetic murine models.
resultsProtein and histological analyses revealed that db/db mice and streptozotocin DN models expressed no significant NET-related proteins, myeloperoxidase, citrullinated histone H3 (citH3), neutrophil elastase, and lymphocyte antigen 6 complex locus G6D (Ly6G). However, the inflamed individuals in the DN model showed that citH3 and Ly6G were highly deposited in the renal system based on immunohistochemistry images. In vitro, NET treatment did not induce apoptosis in glomerular endothelial and renal tubular epithelial cells. NET inhibition by DNase administration demonstrated no significant changes in cell apoptosis.
conclusionsNET-related proteins were only expressed in the DN model with tubulointerstitial inflammation. Our study revealed that NETs are only induced in mice with hyperglycemia-induced inflammation.
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