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The G\u03b1q\/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.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>Methods<\/jats:title>\n            <jats:p>In this study, a murine model of ALI induced by lipopolysaccharide (LPS) was utilized, employing myeloid cell-specific <jats:italic>Gna11<\/jats:italic> 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 G\u03b1q\/11 in ALI. Mouse bone marrow-derived neutrophils were isolated and cultured for live-cell imaging to investigate the in vitro effects of G\u03b1q\/11.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>Results<\/jats:title>\n            <jats:p>The expression of G\u03b1q\/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 <jats:italic>Gna11<\/jats:italic> deficience attenuated LPS-induced lung injury and the formation of NETs in mice. Mechanistically, G\u03b1q\/11 facilitates NETosis by promoting the activation of the endoplasmic reticulum (ER) stress sensor IRE1\u03b1 in neutrophils and mediating the production of mitochondrial reactive oxygen species (mitoROS). Pharmacological inhibition of G\u03b1q\/11 using YM-254,890 was shown to reduce NETs formation and lung injury in mice.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>Conclusions<\/jats:title>\n            <jats:p>The upregulation of G\u03b1q\/11 exacerbates ALI through the promotion of ER stress-mediated NETosis. Consequently, G\u03b1q\/11 represents a potential therapeutic target for the treatment of ALI.<\/jats:p>\n          <\/jats:sec>","DOI":"10.1186\/s10020-025-01118-4","type":"journal-article","created":{"date-parts":[[2025,2,19]],"date-time":"2025-02-19T20:34:51Z","timestamp":1739997291000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":5,"title":["G\u03b1q\/11 aggravates acute lung injury in mice by promoting endoplasmic reticulum stress-mediated NETosis"],"prefix":"10.1186","volume":"31","author":[{"given":"Qian","family":"Xiang","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yang","family":"Tian","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kai","family":"Yang","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yaqin","family":"Du","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jian","family":"Xie","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2025,2,19]]},"reference":[{"key":"1118_CR1","doi-asserted-by":"publisher","first-page":"118740","DOI":"10.1016\/j.lfs.2020.118740","volume":"265","author":"S Bashir","year":"2021","unstructured":"Bashir S, Banday M, Qadri O, Bashir A, Hilal N, Nida IF, Rader S, Fazili KM. 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