ArticleJournal of vascular surgery2016
Effect of DNase I treatment and neutrophil depletion on acute limb ischemia-reperfusion injury in mice.
Article in Journal of vascular surgery, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 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.
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Who cites it
35 citing papers in PubMed, 44 citations in OpenAlex.
- Synthesis, Biological Evaluation, and Molecular Docking of Pyridine-Containing Squaramides as DNase I Inhibitors.Molecules (Basel, Switzerland) · 2026Article
- Review
- Neutrophil-Dominant Inflammatory Responses and Inflammation-Coagulation Burden After Extremity Acute Compartment Syndrome: A Retrospective Multi-Cohort Study.Journal of inflammation research · 2026Article
- Effects of Exercise on Cardiovascular and Metabolic Responses in Adults and Childhood Cancer Survivors: The Role of NETosis and Low-Grade Inflammation as a Novel Therapeutic Target-A Narrative Review.International journal of molecular sciences · 2025Review
- Systemic mechanisms of necrotic cell debris clearance.Cell death & disease · 2024Review
- Neutrophil Extracellular Traps: A Crucial Factor in Post-Surgical Abdominal Adhesion Formation.Cells · 2024Review
- Inhibiting Neutrophil Extracellular Traps Protects against Ultraviolet B-Induced Skin Damage: Effects of Hochu-ekki-to and DNase I.International journal of molecular sciences · 2024Article
- Knockout of the C3a receptor protects against renal ischemia reperfusion injury by reduction of NETs formation.Cellular and molecular life sciences : CMLS · 2023Article
- Genome Engineering of Human Urine-Derived Stem Cells to Express Lactoferrin and Deoxyribonuclease.Tissue engineering. Part A · 2023Article
- Early DNase-I therapy delays secondary brain damage after traumatic brain injury in adult mice.Scientific reports · 2023Article
- Low-density granulocytes in systemic autoimmunity and autoinflammation.Immunological reviews · 2023Review
- Targeting NETs using dual-active DNase1 variants.Frontiers in immunology · 2023Article
- Neutrophil extracellular traps mediate deep vein thrombosis: from mechanism to therapy.Frontiers in immunology · 2023Review
- Inflammatory myopathies and beyond: The dual role of neutrophils in muscle damage and regeneration.Frontiers in immunology · 2023Review
- DNase I and Sivelestat Ameliorate Experimental Hindlimb Ischemia-Reperfusion Injury by Eliminating Neutrophil Extracellular Traps.Journal of inflammation research · 2023Article
- Neutrophils' Extracellular Trap Mechanisms: From Physiology to Pathology.International journal of molecular sciences · 2022Review
- Review
- The role of extracellular traps in ischemia reperfusion injury.Frontiers in immunology · 2022Review
- Analysis of sensitivity and specificity: precise recognition of neutrophils during regeneration of contused skeletal muscle in rats.Forensic sciences research · 2022Article
- Sex Difference in Plasma Deoxyribonuclease Activity in Rats.Physiological research · 2021Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
objectiveExtracellular traps (ETs) consisting of DNA-protein complexes formed after tissue injury contribute to the inflammatory and thrombosis cascades, thereby exacerbating injury. Exogenous DNase I has been suggested as a therapeutic strategy to limit injury in the brain and myocardium. These studies were designed to evaluate the effects of exogenous DNase I treatment on skeletal muscle injury after acute hindlimb ischemia-reperfusion (IR) injury in mice and to determine whether neutrophils are a major source of ETs in postischemic muscle tissue.
methodsC57BL6 mice were subjected to 1.5 hours of tourniquet ischemia and 24 hours of reperfusion with and without human recombinant DNase I treatment. A separate set of mice was subjected to neutrophil depletion (ND), followed by the same intervals of IR. Laser Doppler imaging and tissue harvesting were done at 24 hours for assessment of limb perfusion, muscle fiber injury, adenosine triphosphate (ATP) level, markers of inflammation, thrombosis, and formation of ETs.
resultsDNase I treatment significantly reduced detection of ETs in postischemic muscle but did not alter skeletal muscle fiber injury, levels of proinflammatory molecules, or ATP level. DNase I treatment did enhance postischemic hindlimb perfusion, decreased infiltrating inflammatory cells, and reduced the expression of thrombin-antithrombin III. ND resulted in a significant yet small reduction in ETs in the postischemic muscle. ND did not alter skeletal muscle fiber injury, hindlimb perfusion, or ATP levels.
conclusionsThese data suggest that neither DNase I treatment nor ND was protective against IR injury, even though both decreased detection of ETs in skeletal muscle after IR. Neutrophils are not the only source of ETs after IR.
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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.