ReviewFrontiers in immunology2019
DAMPs and NETs in Sepsis.
Review in Frontiers in immunology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 406 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
406 citing papers in PubMed, 600 citations in OpenAlex.
- Profiling of human and microbial cell-free DNA reflects early host-pathogen interactions in sepsis.Frontiers in immunology · 2026Trial
- Effect of Neutrophil Elastase Inhibitor (Sivelestat Sodium) on Oxygenation in Patients with Sepsis-Induced Acute Respiratory Distress Syndrome.Journal of inflammation research · 2025Trial
- Bilirubin reduces mortality in sepsis models by inhibiting NOX2-mediated formation of neutrophil extracellular traps.Redox report : communications in free radical research · 2026Article
- Extracellular CIRP induces neurotoxic astrocytes via TREM-1 in Alzheimer's disease.bioRxiv : the preprint server for biology · 2026Article
- Review
- Review
- Role of DLL4 in Neutrophil Aging and Impaired Clearance in Sepsis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Article
- Antiviral innate immunity in myocarditis: mechanisms and emerging therapeutics.Experimental & molecular medicine · 2026Review
- Emerging evidence of neutrophil extracellular traps in essential hypertension and target organ damage: pathophysiological insights and therapeutic implications.Hypertension research : official journal of the Japanese Society of Hypertension · 2026Review
- NETs drive CD4⁺ T cell dysfunction in sepsis via mitochondrial ROS and impaired calcium signalling.Molecular medicine (Cambridge, Mass.) · 2026Article
- Single-cell transcriptomic analysis reveals immune remodeling in bone marrow during aged sepsis.GeroScience · 2026Article
- Inflammatory gut-liver crosstalk: mechanisms and therapeutic targets.Experimental & molecular medicine · 2026Review
- Research progress on neutrophil extracellular traps in sepsis‑induced coagulopathy (Review).Molecular medicine reports · 2026Review
- Mitochondrial Immunometabolism in Sepsis: From Oxidative Stress and mtDAMP Signaling to Biomarker-Guided Therapy.International journal of molecular sciences · 2026Review
- A 'Tangled Web' in the CNS: unraveling neutrophil extracellular traps in neurological disorders.Molecular neurodegeneration · 2026Review
- Inhibition of red blood cell-derived small extracellular vesicles release by calpeptin attenuates neutrophil inflammation.Scientific reports · 2026Article
- Neutrophil extracellular traps: A central player in liver diseases.Hepatology communications · 2026Review
- Platelet hyperactivation drives oxidized mitochondrial DNA-induced neutrophil extracellular traps formation in biliary atresia.JHEP reports : innovation in hepatology · 2026Article
- Neutrophil extracellular traps promote macrophage activation through Toll-like receptor engagement and PKA and NF-kB signaling pathways.Cell communication and signaling : CCS · 2026Article
- Neutrophils and Neutrophil Extracellular Traps in Hepatic Ischemia-Reperfusion Injury: Molecular Mechanisms and Therapeutic Strategies.International journal of molecular sciences · 2026Review
346 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 3 institutions in 1 country.
Funding
Abstract
Sepsis is a deadly inflammatory syndrome caused by an exaggerated immune response to infection. Much has been focused on host response to pathogens mediated through the interaction of pathogen-associated molecular patterns (PAMPs) and pattern recognition receptors (PRRs). PRRs are also activated by host nuclear, mitochondrial, and cytosolic proteins, known as damage-associated molecular patterns (DAMPs) that are released from cells during sepsis. Some well described members of the DAMP family are extracellular cold-inducible RNA-binding protein (eCIRP), high mobility group box 1 (HMGB1), histones, and adenosine triphosphate (ATP). DAMPs are released from the cell through inflammasome activation or passively following cell death. Similarly, neutrophil extracellular traps (NETs) are released from neutrophils during inflammation. NETs are webs of extracellular DNA decorated with histones, myeloperoxidase, and elastase. Although NETs contribute to pathogen clearance, excessive NET formation promotes inflammation and tissue damage in sepsis. Here, we review DAMPs and NETs and their crosstalk in sepsis with respect to their sources, activation, release, and function. A clear grasp of DAMPs, NETs and their interaction is crucial for the understanding of the pathophysiology of sepsis and for the development of novel sepsis therapeutics.
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What OpenQuestion 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 OpenQuestion graph.