ReviewRespiratory research2024
Role and intervention of PAD4 in NETs in acute respiratory distress syndrome.
Review in Respiratory research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 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
33 citing papers in PubMed, 37 citations in OpenAlex.
- CAR-engineered neutrophils derived from induced pluripotent stem cells: a new frontier in cellular immunotherapy.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026Review
- Targeting NETosis in the Lung: Respiratory Delivery of Neutrophil-Specific NEBP-Liposomes for Enhanced Therapy of Acute Lung Injury.Molecular pharmaceutics · 2026Article
- Evolution of neutrophil extracellular traps in the pathology of stroke.Neural regeneration research · 2026Article
- Research progress on neutrophil extracellular traps in sepsis‑induced coagulopathy (Review).Molecular medicine reports · 2026Review
- Cell death crosstalk in NET-Driven inflammation: mechanisms, disease contexts, and therapeutic perspectives.Biomarker research · 2026Review
- Correlation analysis of the expression levels of serum endothelial cell adhesion molecule-1 and sirtuin 1 protein in acute respiratory distress syndrome.Journal of medical biochemistry · 2026Article
- Integration of bioinformatics analysis and experimental verification reveals the role of neutrophil extracellular traps in silica nanoparticles-induced lung injury.Journal of nanobiotechnology · 2026Article
- Natural Products Targeting PAD4 in NETosis: Structural and Mechanistic Insights into Direct and Indirect Inhibition.Biomolecules · 2026Review
- Mesenchymal stem cell transplantation alleviated TBI-induced lung injury by inhibiting PAD4-dependent NET formation.Journal of advanced research · 2026Article
- Platelets as Central Modulators of Post-Cardiac Arrest Syndrome: Mechanisms and Therapeutic Implications.Biomolecules · 2026Review
- Phytochemicals as potential inhibitors of NETosis: implications for immunothrombosis and chronic disease management.BMC complementary medicine and therapies · 2026Article
- Neutrophils and neutrophil extracellular traps in ischaemia-reperfusion injury: pathophysiological roles and therapeutic potential.Burns & trauma · 2026Review
- Neutrophil extracellular traps contribute significantly to vascular dysfunction in sepsis.Frontiers in pharmacology · 2026Review
- The Paradox of NET Involvement in the Pathogenesis of Inflammatory Bowel Disease.Inflammatory bowel diseases · 2026Review
- Sepsis-induced immunothrombosis: from cellular crosstalk to multiple organ dysfunction.Frontiers in immunology · 2026Review
- Thirty-five years of evolving inflammatory paradigms in sepsis (1991-2025): a comprehensive mapping of immune dysregulation research, anti-inflammatory targets, and translational barriers.Frontiers in immunology · 2026Article
- Modified Dachengqi Decoction ameliorates sepsis-induced lung injury via the gut microbiota-bile acid axis.Frontiers in cellular and infection microbiology · 2026Article
- Catalpol mitigates rheumatoid arthritis by targeting neutrophil extracellular trap release.Frontiers in immunology · 2026Article
- The Role of Histone Modifications in Acute Lung Injury: Molecular Mechanisms and Potential of Traditional Chinese Medicine Treatment.Journal of inflammation research · 2026Review
- Stroke-Homing Peptide-DNase1 Alleviates Intestinal Ischemia Reperfusion Injury by Selectively Degrading Neutrophil Extracellular Traps.Cell proliferation · 2025Article
Corrections and comments
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Authors and funding
5 authors at 4 institutions in 1 country.
Funding
Abstract
backgroundSepsis is life-threatening organ dysfunction caused by a dysregulated host response to infection. Acute respiratory distress syndrome (ARDS) is a common sepsis-associated injury that can increase postoperative mortality but the mechanism is still unclear. MAIN TEXT: The role of neutrophils in the pathophysiology of sepsis was deeply challenged after the discovery of NETosis, a process resulting in neutrophil extracellular traps (NETs) release. NETs can support thrombin generation and the concept of immunothrombosis has emerged as a new innate response to infection. Immunothrombosis leads to thrombosis in microvessels and supports immune cells together with specific thrombus-related molecules. ARDS is a common sepsis-associated organ injury. Immunothrombosis participates in thrombosis in pulmonary capillaries. Intervention regarding immunothrombosis in ARDS is a key scientific problem. PAD4 is the key enzyme regulating the NET skeleton protein histone H3 to citrulline histone to form NETs in immune thrombosis. This review summarizes NETosis and immunohaemostasis, ARDS and therapeutic opportunities targeting PAD4 via PAD4 inhibitors and lncRNAs potentially, providing future therapies.
conclusionsWe identified and summarized the fundamental definition of ARDS and the concept of immune thrombosis and its composition. NETs activation has become particularly relevant in the formation of immune thrombosis. The taskforce highlighted the intervention targets of PAD4, including noncoding RNAs, potentially providing future therapeutic targets to confront the high postoperative mortality of ARDS.
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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.