ReviewMediators of inflammation2026
Neutrophil Extracellular Traps in Wound Healing of Diabetes: Mechanisms, Inducers, and Therapeutic Implications.
Review in Mediators of inflammation, 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
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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.
- Neutrophil Extracellular Traps in Wound Healing of Diabetes: Mechanisms, Inducers, and Therapeutic Implications.Mediators of inflammation · 2026Review
- De Novo Design Strategies of Nanomedicines for Diabetic Wound Microenvironment Remodeling.BME frontiers · 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
3 authors.
Funding
Abstract
Wound healing damage, especially diabetic foot ulcer (DFU), is a serious complication of diabetes mellitus (DM). New evidence shows that neutrophil extracellular traps (NETs) are the key factor of this pathology. This review summarizes the literature from 2015 to 2024 to clarify the mechanism of NETs and its harmful effects on diabetes wounds. We have provided a detailed introduction to common in vitro NETs inducers such as phorbol 12-myristate 13-acetate (PMA), lipopolysaccharide (LPS), and calcium ionophore, as well as core protein markers such as citrullinated histone H3 (CitH3), myeloperoxidase (MPO), and neutrophil elastase (NE). Importantly, evidence from animal models and human patients suggests that sustained NETs maintain inflammation, hinder angiogenesis, and delay tissue repair. Finally, we explored promising clinical therapeutic strategies that promote healing by targeting NETs, such as DNase I degradation and inhibition of specific signaling pathways, highlighting the potential of NETs inhibition strategies in improving diabetic wound care.
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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.