{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,19]],"date-time":"2026-06-19T00:28:34Z","timestamp":1781828914026,"version":"3.54.5"},"reference-count":37,"publisher":"The Endocrine Society","issue":"11","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2015,11,1]]},"abstract":"<jats:p>Preeclampsia is a pregnancy-specific syndrome characterized by elevated blood pressure, proteinuria, and intrauterine growth restriction (IUGR). Although sterile inflammation appears to be involved, its pathogenesis remains unclear. Recent evidence indicates that sterile inflammation is mediated through the nucleotide-binding oligomerization domain-like receptor family pyrin domain-containing 3 (NLRP3) inflammasomes, composed of NLRP3, apoptosis-associated speck-like protein containing a caspase recruitment domain (ASC), and caspase-1. Here we investigated the role of the NLRP3 inflammasomes in the pathogenesis of preeclampsia using Nlrp3\u2212\/\u2212 and Asc\u2212\/\u2212 (Nlrp3 and Asc deficient) pregnant mice. During pregnancy in mice, continuous infusion of high-dose angiotensin II (AngII) induced hypertension, proteinuria, and IUGR, whereas infusion of low-dose AngII caused hypertension alone. AngII-induced hypertension was prevented in Nlrp3\u2212\/\u2212 mice but not in Asc\u2212\/\u2212, indicating that NLRP3 contributes to gestational hypertension independently of ASC-mediated inflammasomes. Although NLRP3 deficiency had no effect on IUGR, it restored the IL-6 up-regulation in the placenta and kidney of AngII-infused mice. Furthermore, treatment with hydralazine prevented the development of gestational hypertension but not IUGR or IL-6 expression in the placenta and kidney. These findings demonstrate that NLRP3 contributes to the development of gestational hypertension independently of the inflammasomes and that IUGR and kidney injury can occur independent of blood pressure elevation during pregnancy.<\/jats:p>","DOI":"10.1210\/en.2015-1408","type":"journal-article","created":{"date-parts":[[2015,9,11]],"date-time":"2015-09-11T01:02:32Z","timestamp":1441933352000},"page":"4281-4292","source":"Crossref","is-referenced-by-count":66,"title":["NLRP3 Deficiency Improves Angiotensin II-Induced Hypertension But Not Fetal Growth Restriction During Pregnancy"],"prefix":"10.1210","volume":"156","author":[{"given":"Koumei","family":"Shirasuna","sequence":"first","affiliation":[{"name":"Division of Inflammation Research (K.S., T.Ka., F.U., M.K., T.Ko., H.K., A.K., M.T.), Jichi Medical University, Tochigi 329-0498, Japan"},{"name":"Department of Animal Science (K.S.), Tokyo University of Agriculture, Kanagawa 243-0034, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Tadayoshi","family":"Karasawa","sequence":"first","affiliation":[{"name":"Division of Inflammation Research (K.S., T.Ka., F.U., M.K., T.Ko., H.K., A.K., M.T.), Jichi Medical University, Tochigi 329-0498, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Fumitake","family":"Usui","sequence":"first","affiliation":[{"name":"Division of Inflammation Research (K.S., T.Ka., F.U., M.K., T.Ko., H.K., A.K., M.T.), Jichi Medical University, Tochigi 329-0498, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Motoi","family":"Kobayashi","sequence":"first","affiliation":[{"name":"Division of Inflammation Research (K.S., T.Ka., F.U., M.K., T.Ko., H.K., A.K., M.T.), Jichi Medical University, Tochigi 329-0498, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Tadanori","family":"Komada","sequence":"first","affiliation":[{"name":"Division of Inflammation Research (K.S., T.Ka., F.U., M.K., T.Ko., H.K., A.K., M.T.), Jichi Medical University, Tochigi 329-0498, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hiroaki","family":"Kimura","sequence":"first","affiliation":[{"name":"Division of Inflammation Research (K.S., T.Ka., F.U., M.K., T.Ko., H.K., A.K., M.T.), Jichi Medical University, Tochigi 329-0498, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Akira","family":"Kawashima","sequence":"first","affiliation":[{"name":"Division of Inflammation Research (K.S., T.Ka., F.U., M.K., T.Ko., H.K., A.K., M.T.), Jichi Medical University, Tochigi 329-0498, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Akihide","family":"Ohkuchi","sequence":"first","affiliation":[{"name":"Center for Molecular Medicine, Department of Obstetrics and Gynecology (A.O.), Jichi Medical University, Tochigi 329-0498, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Shun\u2019ichiro","family":"Taniguchi","sequence":"first","affiliation":[{"name":"Department of Molecular Oncology (S.T.), Shinshu University Graduate School of Medicine, Nagano 390-8621, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Masafumi","family":"Takahashi","sequence":"first","affiliation":[{"name":"Division of Inflammation Research (K.S., T.Ka., F.U., M.K., T.Ko., H.K., A.K., M.T.), Jichi Medical University, Tochigi 329-0498, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"80","published-online":{"date-parts":[[2015,9,10]]},"reference":[{"key":"2020071612074182000_B1","doi-asserted-by":"crossref","first-page":"247","DOI":"10.1189\/jlb.1112603","article-title":"A leading role for the immune system in the pathophysiology of preeclampsia","volume":"94","author":"Laresgoiti-Servitje","year":"2013","journal-title":"J Leukoc 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