ArticleRedox biology2024
Cathepsin C from extracellular histone-induced M1 alveolar macrophages promotes NETosis during lung ischemia-reperfusion injury.
Article in Redox biology, 2024. 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.
- Autolysosomal enhancer GHF201 attenuates pathophysiology in a mucopolysaccharidosis type I mouse model.Life science alliance · 2026Article
- Review
- Endoplasmic reticulum stress exacerbates ischemia-reperfusion-induced pulmonary endothelial barrier dysfunction by activating TXNDC5.Journal of advanced research · 2026Article
- METTL14-Mediated N6-Methyladenosine Exacerbates Acute Lung Injury via USP30/NCOA4-Dependent Ferroptosis.MedComm · 2026Article
- Increased NETosis in Patients With Heart Failure Is Associated With Macrophage Activation Towards a Proinflammatory Phenotype.Journal of cellular and molecular medicine · 2026Article
- IRF1-mediated sensing of oxidized mitochondrial DNA drives macrophage PANoptosis in lung ischemia-reperfusion injury.Apoptosis : an international journal on programmed cell death · 2026Article
- Chronic stress drives gastric cancer lymph node metastasis via NETosis through a feedforward ACh-NGF axis-mediated PKC-γ/STAT3 pathway.Oncogene · 2026Article
- Necroptosis in alveolar epithelium orchestrates lung ischemia-reperfusion injury: a multi-omics study.Respiratory research · 2026Article
- A 'Tangled Web' in the CNS: unraveling neutrophil extracellular traps in neurological disorders.Molecular neurodegeneration · 2026Review
- Cathepsin C Restricts Influenza A Virus Replication and Is Associated with Suppression of the PI3K-AKT Signaling Pathway.Viruses · 2026Article
- GPNMB modulates neutrophil extracellular trap formation: therapeutic implications for ischemic stroke.Journal of neuroinflammation · 2026Article
- Emerging biomodels to understand the pathophysiology of sepsis and evaluate new therapeutic strategies targeting extracellular histones.Materials today. Bio · 2026Review
- WWC1 deficiency exacerbates sepsis-induced lung injury by promoting NETosis, M1 and M2b macrophage recruitment, and pyroptosis via YAP1 and STING pathways.Journal of inflammation (London, England) · 2026Article
- Damage-Associated Molecular Patterns in Perioperative Anesthesia Care: A Clinical Perspective.Anesthesia research · 2026Article
- Mesenchymal stem cell transplantation alleviated TBI-induced lung injury by inhibiting PAD4-dependent NET formation.Journal of advanced research · 2026Article
- Dynamic regulation and targeted interventions of macrophages in ischemia-reperfusion injury.Journal of advanced research · 2026Review
- Unveiling Interleukin-40: A Novel Regulator of Macrophage and B Cell Function in Allergic Asthma.International journal of biological sciences · 2026Article
- Neutrophil extracellular traps contribute significantly to vascular dysfunction in sepsis.Frontiers in pharmacology · 2026Review
- Neutrophil-macrophage crosstalk network in acute lung injury: feedback circuits linking cytokine storm and cell death.Frontiers in cellular and infection microbiology · 2026Review
- Endothelial Senescence-Associated Secretory Signaling Promotes Macrophage Extracellular Traps Formation and Contributes to the Exacerbation of Combined Lung Injury.International journal of biological sciences · 2026Article
Corrections and comments
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Authors and funding
9 authors.
Funding
Abstract
Primary graft dysfunction (PGD) is a severe form of acute lung injury resulting from lung ischemia/reperfusion injury (I/R) in lung transplantation (LTx), associated with elevated post-transplant morbidity and mortality rates. Neutrophils infiltrating during reperfusion are identified as pivotal contributors to lung I/R injury by releasing excessive neutrophil extracellular traps (NETs) via NETosis. While alveolar macrophages (AMs) are involved in regulating neutrophil chemotaxis and infiltration, their role in NETosis during lung I/R remains inadequately elucidated. Extracellular histones constitute the main structure of NETs and can activate AMs. In this study, we confirmed the significant involvement of extracellular histone-induced M1 phenotype of AMs (M1-AMs) in driving NETosis during lung I/R. Using secretome analysis, public protein databases, and transwell co-culture models of AMs and neutrophils, we identified Cathepsin C (CTSC) derived from AMs as a major mediator in NETosis. Further elucidating the molecular mechanisms, we found that CTSC induced NETosis through a pathway dependent on NADPH oxidase-mediated production of reactive oxygen species (ROS). CTSC could significantly activate p38 MAPK, resulting in the phosphorylation of the NADPH oxidase subunit p47
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