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Second, G\u03b1q was activated in mouse placenta using Cre-lox and DREADD methodologies. Syncytiotrophoblast-restricted G\u03b1q activation caused hypertension, kidney damage, proteinuria, elevated circulating proinflammatory factors, decreased placental vascularization, diminished spiral artery diameter, and augmented responses to mitochondrial-derived superoxide. Administration of the mitochondrial-targeted antioxidant Mitoquinone attenuated maternal proteinuria, lowered circulating inflammatory and anti-angiogenic mediators, and maintained placental vascularization. These data demonstrate a causal relationship between syncytiotrophoblast stress and the development of preeclampsia and identify elevated G\u03b1q signaling and mitochondrial reactive oxygen species as a cause of this stress.<\/jats:p>","DOI":"10.1126\/sciadv.adg8118","type":"journal-article","created":{"date-parts":[[2023,12,1]],"date-time":"2023-12-01T18:58:36Z","timestamp":1701457116000},"update-policy":"https:\/\/doi.org\/10.34133\/aaas_crossmark","source":"Crossref","is-referenced-by-count":19,"title":["Mitochondrial-targeted antioxidant attenuates preeclampsia-like phenotypes induced by syncytiotrophoblast-specific G\u03b1q signaling"],"prefix":"10.1126","volume":"9","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-2961-8977","authenticated-orcid":true,"given":"Megan A.","family":"Opichka","sequence":"first","affiliation":[{"name":"Department of Physiology, Medical College of Wisconsin, Milwaukee, USA."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"M. 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