ArticleBlood2022
Liver-to-lung microembolic NETs promote gasdermin D-dependent inflammatory lung injury in sickle cell disease.
Article in Blood, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.
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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
50 citing papers in PubMed, 61 citations in OpenAlex.
- Haemolytic injury and cardiovascular disease.Nature reviews. Cardiology · 2026Review
- Acute therapy with hemopexin (CSL889) resolves LPS-induced lung vaso-occlusion in sickle mice.Blood vessels, thrombosis & hemostasis · 2026Article
- A 'Tangled Web' in the CNS: unraveling neutrophil extracellular traps in neurological disorders.Molecular neurodegeneration · 2026Review
- Sickle cell visualization in vivo in humans: microvascular occlusion formation and hemorheological indices.Blood advances · 2026Article
- Lights, camera, occlusion! watch sickle cells in real time.Blood advances · 2026Article
- Review
- Proteomic Analysis of Golden Sputum Reveals Pulmonary Complement Activation During Acute Chest Syndrome in Children With Sickle Cell Disease.American journal of hematology · 2026Article
- Intravenous immunoglobulins in the management of acute chest syndrome in two Jehovah's Witnesses with sickle cell disease.Haematologica · 2026Article
- CD39 polymorphism enables lung thrombosis in sickle cell disease.Nature communications · 2026Article
- One trigger, two fates: hemolysate shapes neutrophil extracellular traps (NETs) formation in a context-dependent manner.Frontiers in immunology · 2026Article
- crizanlizumab and inclacumab are equally potent inhibitors of cell adhesion in the blood of patients with sickle cell disease.Blood. Red cells & iron · 2025Article
- αIIbβ3-dependent platelet procoagulant activity promotes pulmonary arterial thrombosis triggered by circulating tissue factor.Thrombosis research · 2025Article
- Hepatic ischemia-reperfusion injury: Underlying mechanisms and concepts in liver surgery and liver transplantation.Hepatology (Baltimore, Md.) · 2025Article
- Emerging pathways in thromboinflammation of sickle cell disease: novel findings in disease pathogenesis.Research and practice in thrombosis and haemostasis · 2025Review
- Next-Generation Regenerative Therapies for Alpha-1 Antitrypsin Deficiency: Molecular Pathogenesis to Clinical Translation.International journal of molecular sciences · 2025Review
- Crosstalk between lung and extrapulmonary organs in sepsis-related acute lung injury/acute respiratory distress syndrome.Annals of intensive care · 2025Review
- GSDMD-mediated pyroptosis: molecular mechanisms, diseases and therapeutic targets.Molecular biomedicine · 2025Review
- Sepsis-induced NET formation requires MYD88 but is independent of GSDMD and PAD4.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- Dynamics of neutrophil phenotype and function in sickle cell disease.Frontiers in immunology · 2025Article
- GSDMD-NETs in patients with sepsis-induced coagulopathy and their interaction with glycocalyx damage.Frontiers in immunology · 2025Article
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12 authors at 1 institution in 1 country.
Funding
Abstract
Acute lung injury, referred to as the acute chest syndrome, is a major cause of morbidity and mortality in patients with sickle cell disease (SCD), which often occurs in the setting of a vaso-occlusive painful crisis. P-selectin antibody therapy reduces hospitalization of patients with SCD by ∼50%, suggesting that an unknown P-selectin-independent mechanism promotes remaining vaso-occlusive events. In patients with SCD, intraerythrocytic polymerization of mutant hemoglobin promotes ischemia-reperfusion injury and hemolysis, which leads to the development of sterile inflammation. Using intravital microscopy in transgenic, humanized mice with SCD and in vitro studies with blood from patients with SCD, we reveal for the first time that the sterile inflammatory milieu in SCD promotes caspase-4/11-dependent activation of neutrophil-gasdermin D (GSDMD), which triggers P-selectin-independent shedding of neutrophil extracellular traps (NETs) in the liver. Remarkably, these NETs travel intravascularly from liver to lung, where they promote neutrophil-platelet aggregation and the development of acute lung injury. This study introduces a novel paradigm that liver-to-lung embolic translocation of NETs promotes pulmonary vascular vaso-occlusion and identifies a new GSDMD-mediated, P-selectin-independent mechanism of lung injury in SCD.
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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.