ArticleFrontiers in immunology2023
Targeting NETs using dual-active DNase1 variants.
Article in Frontiers in immunology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed, 46 citations in OpenAlex.
- Improvement of the Purification Process for Earthworm DNase and Cytotoxicity Analysis.The protein journal · 2026Article
- Review
- Hyperacute Interleukin-1β Production and Neutrophil Extracellular Trap Formation in the Cerebral Circulation of Stroke Patients with Large Vessel Occlusion.Annals of neurology · 2026Article
- Nanomaterials-Based Immunotherapy for Atherosclerosis.Small (Weinheim an der Bergstrasse, Germany) · 2026Review
- Immune response to DNA and RNA: structural insights, molecular mechanisms, and therapeutic targeting.Molecular biomedicine · 2026Review
- Impact of Neutrophil Extracellular Traps on Clinical Outcome after Subarachnoid Hemorrhage: A Translational Narrative Review.Translational stroke research · 2026Review
- Spatiotemporal heterogeneity of neutrophil extracellular traps in hepatocellular carcinoma microenvironment and targeted therapy progress.Journal of translational medicine · 2026Review
- DNase1 RS1053874 Polymorphism is Associated with Early Neurological Recovery through NET Modulation and with Long-Term Survival in Ischemic Stroke: A Prospective Cohort Study.Annals of neurology · 2026Observational
- Neutrophil-Mimetic Nanoscavengers Target the Inflammatory Microenvironment to Eliminate NETs/ROS and Immunomodulate cGAS-STING Signaling in Septic AKI.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Role of neutrophils in regulating vascular permeability in inflammatory and autoimmune diseases.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Review
- NAC and DNase I synergistically reduce NETs to attenuate severe acute pancreatitis via suppressing the NETs/NF-κB/CXCL3 pathway.Apoptosis : an international journal on programmed cell death · 2026Article
- Neutrophil extracellular traps in gout: from immune defense to pathological dynamic equilibrium.Frontiers in immunology · 2026Review
- Mechanistic interplay between extracellular vesicles and neutrophil extracellular traps: unveiling the "sterile inflammation" cascade in obesity-induced diabetes progression.Frontiers in immunology · 2026Review
- Ensnarement of Stressed Macrophages by NETs in Atherosclerosis.Circulation research · 2025Article
- Macrophage DNases Limit Neutrophil Extracellular Trap-Mediated Defective Efferocytosis in Atherosclerosis.Circulation research · 2025Article
- Stroke-Homing Peptide-DNase1 Alleviates Intestinal Ischemia Reperfusion Injury by Selectively Degrading Neutrophil Extracellular Traps.Cell proliferation · 2025Article
- NETosis in myocardial ischemia-reperfusion injury: From mechanisms to therapies (Review).Biomedical reports · 2025Review
- CitH3, a Druggable Biomarker for Human Diseases Associated with Acute NETosis and Chronic Immune Dysfunction.Pharmaceutics · 2025Review
- Constructing of Synthetic DNA-Histone Networks as Extracellular Trap Model for Biomedical Research.Bulletin of experimental biology and medicine · 2025Article
- A Web of Challenges: The Therapeutic Struggle to Target NETs in Disease.International journal of molecular sciences · 2025Review
Corrections and comments
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Authors and funding
17 authors at 8 institutions in 6 countries.
Funding
Abstract
Background: Neutrophil Extracellular Traps (NETs) are key mediators of immunothrombotic mechanisms and defective clearance of NETs from the circulation underlies an array of thrombotic, inflammatory, infectious, and autoimmune diseases. Efficient NET degradation depends on the combined activity of two distinct DNases, DNase1 and DNase1-like 3 (DNase1L3) that preferentially digest double-stranded DNA (dsDNA) and chromatin, respectively. Methods: Here, we engineered a dual-active DNase with combined DNase1 and DNase1L3 activities and characterized the enzyme for its NET degrading potential in vitro. Furthermore, we produced a mouse model with transgenic expression of the dual-active DNase and analyzed body fluids of these animals for DNase1 and DNase 1L3 activities. We systematically substituted 20 amino acid stretches in DNase1 that were not conserved among DNase1 and DNase1L3 with homologous DNase1L3 sequences. Results: We found that the ability of DNase1L3 to degrade chromatin is embedded into three discrete areas of the enzyme's core body, not the C-terminal domain as suggested by the state-of-the-art. Further, combined transfer of the aforementioned areas of DNase1L3 to DNase1 generated a dual-active DNase1 enzyme with additional chromatin degrading activity. The dual-active DNase1 mutant was superior to native DNase1 and DNase1L3 in degrading dsDNA and chromatin, respectively. Transgenic expression of the dual-active DNase1 mutant in hepatocytes of mice lacking endogenous DNases revealed that the engineered enzyme was stable in the circulation, released into serum and filtered to the bile but not into the urine. Conclusion: Therefore, the dual-active DNase1 mutant is a promising tool for neutralization of DNA and NETs with potential therapeutic applications for interference with thromboinflammatory disease states.
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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 OpenQuestion graph.