ArticleMolecular medicine (Cambridge, Mass.)2025
Gαq/11 aggravates acute lung injury in mice by promoting endoplasmic reticulum stress-mediated NETosis.
Article in Molecular medicine (Cambridge, Mass.), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Endoplasmic reticulum stress and the unfolded protein response in lung diseases: molecular pathways and therapeutic interventions.The Journal of pathology · 2026Review
- Neutrophil Extracellular Traps in Diabetic Kidney Disease: Mechanisms of Pathogenesis and Emerging Therapeutic Strategies.Drug design, development and therapy · 2026Review
- New Exploration of Therapeutic Targets for Radiation Pneumonitis: Comparative Analysis of Molecular Pathways in Radiation-Induced and LPS-Induced Pneumonitis.International journal of medical sciences · 2025Review
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5 authors.
Funding
Abstract
backgroundAcute lung injury (ALI) is distinguished by exaggerated neutrophil extracellular traps (NETs), elevated clinical mortality rates, and a paucity of targeted therapeutic interventions. The Gαq/11 protein, a member of the G protein subfamily, is an effective intervention target for a variety of diseases, but little is known about its role in ALI.
methodsIn this study, a murine model of ALI induced by lipopolysaccharide (LPS) was utilized, employing myeloid cell-specific Gna11 knockout mice. The pulmonary pathology of mice was assessed and the lung samples were collected for immunofluorescence staining and RNA-sequencing analysis to elucidate the impact and underlying mechanisms of Gαq/11 in ALI. Mouse bone marrow-derived neutrophils were isolated and cultured for live-cell imaging to investigate the in vitro effects of Gαq/11.
resultsThe expression of Gαq/11 was found to be upregulated in the lung tissues of mice with ALI, coinciding with the increased expression of inflammatory genes. Myeloid cell-specific Gna11 deficience attenuated LPS-induced lung injury and the formation of NETs in mice. Mechanistically, Gαq/11 facilitates NETosis by promoting the activation of the endoplasmic reticulum (ER) stress sensor IRE1α in neutrophils and mediating the production of mitochondrial reactive oxygen species (mitoROS). Pharmacological inhibition of Gαq/11 using YM-254,890 was shown to reduce NETs formation and lung injury in mice.
conclusionsThe upregulation of Gαq/11 exacerbates ALI through the promotion of ER stress-mediated NETosis. Consequently, Gαq/11 represents a potential therapeutic target for the treatment of ALI.
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