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Molecular Mechanisms of Neutrophil Extracellular Traps (Nets) in Human Diseases
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Molecular Mechanisms of Neutrophil Extracellular Traps (Nets) in Human Diseases

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: 20 August 2026 | Viewed by 6853

Special Issue Editor

Dr. Eisuke F. Sato

E-Mail Website
Guest Editor
Department of Biochemistry, Faculty of Pharmaceutical Sciences, Suzuka University of Medical Science, 3500-3, Minamitamagaki, Suzuka City 513-8670, Mie, Japan
Interests: neutrophil extracellular trap; neutrophil

Special Issue Information

Dear Colleagues,

Neutrophil extracellular traps (NETs), released by activated neutrophils, play a crucial role in various human diseases, including sepsis, multi-drug resistant infections, autoimmune disorders, cardiovascular diseases, and cancer. Excessive or dysregulated NET formation contributes to tissue damage, inflammation, and thrombosis. In autoimmune diseases like systemic lupus erythematosus and rheumatoid arthritis, NETs serve as autoantigens, sustaining the autoimmune response. In cardiovascular diseases, they promote thrombus formation and atherosclerosis progression, while in cancer, they facilitate tumor metastasis and a pro-tumorigenic microenvironment.

Despite their recognized pathological roles, the precise mechanisms regulating NET formation and clearance remain unclear. Further research is needed to understand the triggers, signaling pathways, and degradation mechanisms of NETs, as well as their therapeutic potential. This Special Issue aims to consolidate current knowledge on NETs in human diseases, highlighting molecular mechanisms and clinical relevance through original research and review articles.

Dr. Eisuke F. Sato
Guest Editor

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Keywords

  • neutrophil extracellular traps (NETs)
  • neutrophils
  • inflammation
  • autoimmune diseases
  • cardiovascular diseases
  • tumor metastasis
  • thrombosis
  • molecular mechanisms
  • disease progression
  • therapeutic targets

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Published Papers (3 papers)

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Research

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16 pages, 4165 KB  
Article
Hispidin Ameliorates Acute Ultraviolet B-Induced Skin Inflammation by Targeting Reactive Oxygen Species-Dependent Neutrophil Extracellular Trap Formation
by Yuina Arakaki, Koshi Tominaga, Keiichi Hiramoto, Masashi Imai, Akihiro Morita, Tomonari Tsutsumi, Hiroyuki Yasuda and Eisuke F. Sato
Int. J. Mol. Sci. 2026, 27(8), 3667; https://doi.org/10.3390/ijms27083667 - 20 Apr 2026
Viewed by 148
Abstract
Excessive neutrophil extracellular trap (NET) formation (NETosis), frequently associated with reactive oxygen species (ROS), exacerbates cutaneous inflammation induced by acute ultraviolet B (UVB) exposure. Although hispidin has potent antioxidant activity, its protective effects against acute UVB-induced skin inflammation and its relationship with NET-associated [...] Read more.
Excessive neutrophil extracellular trap (NET) formation (NETosis), frequently associated with reactive oxygen species (ROS), exacerbates cutaneous inflammation induced by acute ultraviolet B (UVB) exposure. Although hispidin has potent antioxidant activity, its protective effects against acute UVB-induced skin inflammation and its relationship with NET-associated responses remain unclear. We investigated the effects of topical hispidin on acute UVB-induced skin injury in mice and examined its effects on ROS-associated NET-related responses in differentiated HL-60 cells. In a mouse model, topical hispidin (0.1% and 0.5%) ameliorated UVB-induced skin damage in a dose-dependent manner, as evidenced by improved clinical and histological findings. Hispidin treatment was associated with reduced systemic oxidative stress and decreased cutaneous expression of CXCL2, C5a, IL-1β, NLRP3, Ly6G, PAD4, and citrullinated histone H3. In differentiated HL-60 cells, hispidin reduced ROS-associated signals and suppressed PMA-triggered extracellular DNA release, but did not suppress A23187-triggered extracellular DNA release under experimental conditions. Cell viability analysis showed that hispidin did not significantly affect differentiated HL-60 cell viability at tested concentrations under the present experimental conditions. Topical hispidin alleviates acute UVB-induced skin inflammation by suppressing neutrophil infiltration and NET-related inflammatory responses. Hispidin may therefore represent a promising candidate as a topical modulator of oxidative stress- and NET-associated skin inflammation. Full article
(This article belongs to the Special Issue Molecular Mechanisms of Neutrophil Extracellular Traps (Nets) in Human Diseases)
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13 pages, 254 KB  
Article
NETosis Markers (ssDNA, dsDNA) as Predictors of Mortality and Hospitalization After Endovascular Aortic Repair
by Milena N. Michalska, Tadeusz Grochowiecki, Aleksandra Wyczałkowska-Tomasik, Leszek Pączek, Michał Macech, Bartłomiej Antoń and Zbigniew Gałązka
Int. J. Mol. Sci. 2026, 27(5), 2427; https://doi.org/10.3390/ijms27052427 - 6 Mar 2026
Viewed by 380
Abstract
Neutrophils and their extracellular traps (NETs) are pivotal elements of the immune response. This study investigates the dynamics of neutrophil-related markers during the perioperative period of branched endovascular aortic repair (BEVAR) in patients with thoracoabdominal aortic aneurysms (TAAAs) and evaluates their association with [...] Read more.
Neutrophils and their extracellular traps (NETs) are pivotal elements of the immune response. This study investigates the dynamics of neutrophil-related markers during the perioperative period of branched endovascular aortic repair (BEVAR) in patients with thoracoabdominal aortic aneurysms (TAAAs) and evaluates their association with one-year clinical outcomes. A prospective, single-center study was conducted on 20 TAAA patients treated with T-branch devices. The analysis focused on surrogate markers associated with NETosis, including double-stranded DNA (dsDNA), single-stranded DNA (ssDNA), and citrullinated histone H3 (citH3). Peripheral venous blood was collected 24 h before BEVAR, and on the third and fifth postoperative days. Patients were monitored for one year to evaluate mortality and hospitalization risks, with predictors identified using Cox regression analysis. Increased postoperative levels of inflammatory markers were significantly associated with higher risks of mortality and hospital readmission. On the third postoperative day, key parameters emerged as predictors of adverse outcomes: dsDNA (HR = 1.000; 95% CI 1.000–1.000; p = 0.027), ssDNA (HR = 1.000; 95% CI 1.000–1.000; p = 0.022), and NLR (HR = 1.226; 95% CI 1.043–1.440; p = 0.013). Markers assessed in the early postoperative period (the third postopearive day) demonstrated superior predictive utility compared to those measured on the fifth postoperative day. CitH3 levels did not show statistical significance as a prognostic factor. Early postoperative evaluation of NET-associated markers, particularly dsDNA and ssDNA, offers prognostic value for predicting mortality and hospitalization risks in TAAA patients undergoing BEVAR. These markers may provide superior predictive accuracy compared to conventional post-implantation syndrome criteria. Enhanced postoperative monitoring of these markers could help identify high-risk patients who may benefit from intensified follow-up. Full article
(This article belongs to the Special Issue Molecular Mechanisms of Neutrophil Extracellular Traps (Nets) in Human Diseases)

Review

Jump to: Research

29 pages, 1710 KB  
Review
A Web of Challenges: The Therapeutic Struggle to Target NETs in Disease
by Andre Espiritu and Kim Maree O’Sullivan
Int. J. Mol. Sci. 2025, 26(10), 4773; https://doi.org/10.3390/ijms26104773 - 16 May 2025
Cited by 14 | Viewed by 5807
Abstract
Neutrophil extracellular traps (NETs) play a crucial role in the pathophysiology of many debilitating conditions, including autoimmune diseases, inflammatory diseases, and cancer. As a result, NET-targeted therapies have been investigated in search of effective treatment strategies. Despite promising preclinical findings, clinical translation of [...] Read more.
Neutrophil extracellular traps (NETs) play a crucial role in the pathophysiology of many debilitating conditions, including autoimmune diseases, inflammatory diseases, and cancer. As a result, NET-targeted therapies have been investigated in search of effective treatment strategies. Despite promising preclinical findings, clinical translation of NET inhibitors has had limited success. These preclinical studies have faced limitations such as mouse models that inaccurately reflect human disease dynamics, as well as by the complexity of NETs—including their diverse morphology and convoluted pathways to formation relative to pathology. The NET inhibitors themselves have several limitations, including off-target effects and bioavailability issues. The challenges facing NET-targeted therapies reported here may explain what is required to go from bench to bedside successfully. Full article
(This article belongs to the Special Issue Molecular Mechanisms of Neutrophil Extracellular Traps (Nets) in Human Diseases)
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