{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,2]],"date-time":"2026-09-02T06:17:45Z","timestamp":1788329865967,"version":"build-2803163510"},"reference-count":89,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"17","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["JAHA"],"published-print":{"date-parts":[[2026,9,1]]},"abstract":"<jats:sec xml:lang=\"en\">\n                    <jats:title>Background<\/jats:title>\n                    <jats:p xml:lang=\"en\">Pregnancy complications such as preeclampsia and fetal growth restriction are caused by compromised placentation associated with impaired maternal cardiovascular and immune adaptation to pregnancy, but the pathophysiological pathways underlying these impairments are not fully defined. C1q (complement component 1q) plays a central role in immune cell recruitment, functional regulation, and immune tolerance. In this study, we investigated the impact of maternal C1q deficiency on maternal uterine and systemic cardiovascular parameters in pregnancy.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec xml:lang=\"en\">\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p xml:lang=\"en\">\n                      <jats:italic toggle=\"no\">C1q<\/jats:italic>\n                      null mutant (\n                      <jats:italic toggle=\"no\">C1qa<\/jats:italic>\n                      <jats:sup>\u2212\/\u2212<\/jats:sup>\n                      ) and C57BL\/6 wild\u2010type control female mice were mated with BALB\/c males. Cardiovascular adaptations were investigated by echocardiography and wire myography, as well as uterine artery ultrasound and decidual spiral artery assessment.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec xml:lang=\"en\">\n                    <jats:title>Results<\/jats:title>\n                    <jats:p xml:lang=\"en\">\n                      <jats:italic toggle=\"no\">C1qa<\/jats:italic>\n                      <jats:sup>\u2212\/\u2212<\/jats:sup>\n                      dams exhibited increased fetal loss (\u21913.6\u2010fold;\n                      <jats:italic toggle=\"no\">P<\/jats:italic>\n                      =0.011) and late gestation fetal growth restriction, notably among male fetuses (\n                      <jats:italic toggle=\"no\">P<\/jats:italic>\n                      =0.002). Mesenteric arteries from\n                      <jats:italic toggle=\"no\">C1qa<\/jats:italic>\n                      <jats:sup>\u2212\/\u2212<\/jats:sup>\n                      dams displayed heightened vasoconstriction ex\u00a0vivo (area under the curve \u219134%;\n                      <jats:italic toggle=\"no\">P<\/jats:italic>\n                      =0.018). In midpregnancy,\n                      <jats:italic toggle=\"no\">C1qa<\/jats:italic>\n                      <jats:sup>\u2212\/\u2212<\/jats:sup>\n                      dams exhibited uterine artery dysfunction (resistance index \u219123%;\n                      <jats:italic toggle=\"no\">P<\/jats:italic>\n                      =0.014), defective decidual spiral artery remodeling (vessel wall thickness: \u219116%;\n                      <jats:italic toggle=\"no\">P<\/jats:italic>\n                      =0.010), and reduced decidual perivascular macrophages surrounding spiral arteries (\u219328%;\n                      <jats:italic toggle=\"no\">P<\/jats:italic>\n                      =0.050) compared with control dams.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec xml:lang=\"en\">\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p xml:lang=\"en\">These findings indicate that maternal C1q deficiency disrupts key cardiovascular adaptations to pregnancy, likely contributing to poor fetal outcomes via impaired maternal hemodynamics and constrained placental function. This study identifies maternal C1q as a critical regulator of pregnancy\u2010induced vascular adaptation and supports mounting evidence for C1q relevance in pregnancy complications involving placental insufficiency.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1161\/jaha.125.048023","type":"journal-article","created":{"date-parts":[[2026,8,27]],"date-time":"2026-08-27T11:14:59Z","timestamp":1787829299000},"update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":0,"title":["Complement Component 1q Deficiency Impairs Maternal Hemodynamic Adaptations to Pregnancy, Decidual Vascular Remodeling, and Fetal Growth in Mice"],"prefix":"10.1161","volume":"15","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-1914-2095","authenticated-orcid":false,"given":"Evangeline A. 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Australia"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-6990-8883","authenticated-orcid":false,"given":"Shanna L.","family":"Hosking","sequence":"additional","affiliation":[{"name":"Robinson Research Institute and the School of Pharmacy and Biomedical Sciences, Adelaide University","place":["Adelaide, Australia"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-3141-2521","authenticated-orcid":false,"given":"Lachlan M.","family":"Moldenhauer","sequence":"additional","affiliation":[{"name":"Robinson Research Institute and the School of Pharmacy and Biomedical Sciences, Adelaide University","place":["Adelaide, Australia"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Holly M.","family":"Groome","sequence":"additional","affiliation":[{"name":"Robinson Research Institute and the School of Pharmacy and Biomedical Sciences, Adelaide University","place":["Adelaide, 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