ArticleiScience2025
Cathepsin C-driven enhancement of neutrophil extracellular trap formation contributes to acute lung injury.
Article in iScience, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 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
3 citing papers in PubMed.
- Alveolar macrophage-neutrophil crosstalk in acute lung injury: mechanisms, feedback loops, and therapeutic opportunities.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Review
- Neutrophil-macrophage crosstalk network in acute lung injury: feedback circuits linking cytokine storm and cell death.Frontiers in cellular and infection microbiology · 2026Review
- Interactions between neutrophil extracellular traps and macrophages: the key to inflammatory diseases.Frontiers in immunology · 2026Review
Corrections and comments
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Authors and funding
14 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Acute lung injury (ALI) is a severe pulmonary inflammatory disease with high morbidity and mortality rates. The pulmonary inflammatory phenotype of ALI is driven by the excessive aggregation and activation of neutrophils, triggering a cytokine storm. Notably, the extensive formation of neutrophil extracellular traps (NETs) has been demonstrated to play a critical role in ALI. Our results revealed significant overexpression of Cathepsin C (CTSC) in macrophages after LPS stimulation, which subsequently promoted massive NET formation through a positive feedback mechanism. Specifically, LPS stimulation markedly elevated CTSC expression in macrophages, which subsequently promoted the autocrine secretion of CTSC from neutrophils, ultimately culminating in excessive NET formation through the activation of the PR3-IL-1β-p38 pathway. Consequently, the inhibition of CTSC or PR3 significantly reduced NET formation and attenuated lung injury in ALI mice. In summary, CTSC overexpression drives excessive NET formation in ALI mice through a neutrophil-mediated positive feedback loop regulated by the PR3-IL-1β-p38 pathway.
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Registered trials
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