ReviewDrug design, development and therapy2026
Neutrophil Extracellular Traps in Diabetic Kidney Disease: Mechanisms of Pathogenesis and Emerging Therapeutic Strategies.
Review in Drug design, development and therapy, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
2 citing papers in PubMed.
- Neutrophils in Kidney Disease: Linking Neutrophil Function and Microenvironment to Therapeutic Targets.Journal of inflammation research · 2026Review
- Study on the pro-inflammatory injury of neutrophil extracellular traps in gouty nephropathy.Frontiers in immunology · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Diabetic kidney disease (DKD) is a major microvascular complication of diabetes mellitus and the leading global cause of end-stage renal disease. While chronic hyperglycemia and classic metabolic pathways such as protein kinase C activation, advanced glycation end product (AGE) accumulation, and renin-angiotensin system overactivity elucidate many features of DKD, they do not fully account for its complex inflammatory pathology. Recent studies have highlighted neutrophil extracellular trap (NET) formation, or NETosis, as a critical mechanism linking metabolic stress to immune dysregulation in DKD. NETosis is a specialized form of programmed cell death in neutrophils that releases web-like chromatin structures decorated with histones, elastase, and myeloperoxidase. Although these structures function as protective barriers against pathogens, they become pathogenic when dysregulated. In the diabetic milieu, hyperglycemia, advanced glycation end products (AGEs), protein kinase C signaling, lipid abnormalities, and pro-inflammatory cytokines all promote excessive NETosis. Once formed, NETs drive renal injury by inducing endothelial dysfunction, podocyte and tubular epithelial cell damage, macrophage activation, and profibrotic signaling, thereby accelerating inflammation, fibrosis, and renal decline. Therapeutic strategies targeting NETosis are emerging, including inhibitors of PAD4, NADPH oxidase, and neutrophil elastase, as well as NET-degrading agents such as DNase I and histone-neutralizing compounds. Classical antidiabetic drugs, notably metformin and GLP-1 receptor agonists, also show potential in modulating NET formation. Collectively, these insights position NETosis as both a biomarker and a therapeutic target in DKD, offering novel opportunities to mitigate diabetes-associated renal complications.
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What Socratic holds
Registered trials
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.