{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,3,1]],"date-time":"2026-03-01T06:16:27Z","timestamp":1772345787734,"version":"3.50.1"},"reference-count":62,"publisher":"Oxford University Press (OUP)","issue":"4","license":[{"start":{"date-parts":[[2023,2,4]],"date-time":"2023-02-04T00:00:00Z","timestamp":1675468800000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by-nc\/4.0\/"}],"funder":[{"DOI":"10.13039\/501100001511","name":"Auckland Medical Research Foundation","doi-asserted-by":"publisher","award":["1320002"],"award-info":[{"award-number":["1320002"]}],"id":[{"id":"10.13039\/501100001511","id-type":"DOI","asserted-by":"publisher"}]},{"name":"Royal Society of New Zealand Marsden","award":["20-UOA-002"],"award-info":[{"award-number":["20-UOA-002"]}]},{"name":"Genotype-Tissue Expression"},{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000054","name":"National Cancer Institute","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100000054","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000051","name":"National Human Genome Research Institute","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100000051","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000050","name":"National Heart, Lung, and Blood Institute","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100000050","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100010232","name":"National Institute of Development Administration","doi-asserted-by":"publisher","id":[{"id":"10.13039\/501100010232","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000025","name":"National Institute of Mental Health","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100000025","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000065","name":"National Institute of Neurological Disorders and Stroke","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100000065","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2023,4,11]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>Preeclampsia (PE) is a relatively common but severe pregnancy disorder (with very limited effective treatments) characterized by hypertension (HTN) and usually proteinuria (PRO) or other organ damage. Genome-wide association studies (GWAS) of PE, HTN, and PRO have mostly identified risk loci single nucleotide polymorphisms (SNPs) located in noncoding genomic regions, likely impacting the regulation of distal gene expression. The latest GWAS associated (P\u2009&amp;lt;\u20091 \u00d7 10\u22126) SNPs to PE (n\u2009=\u200925), HTN (n\u2009=\u20091926), and PRO (n\u2009=\u2009170). Our algorithmic analysis (CoDeS3D) used chromatin connection data (Hi-C) derived from 70 cell lines followed by analysis of two expression quantitative trail loci (eQTL) cohorts: GTEx (838 donors, 54 tissues, totaling 15 253 samples) and DICE (91 donors, 13 blood tissue types). We identified spatially constrained eQTLs which implicate gene targets in PE (n\u2009=\u200916), HTN (n\u2009=\u20093561), and PRO (n\u2009=\u2009335). By overlapping these target genes and their molecular pathways (protein\u2013protein interaction networks), we identified shared functional impacts between PE and HTN, which are significantly enriched for regulatory interactions which target genes intolerant to loss-of-function mutations. While the disease-associated SNP loci mostly do not overlap, the regulatory signals (target genes and pathways) overlap, informing on PE risk mechanisms. This demonstrates a model in which genetic predisposition to HTN and PRO lays a molecular groundwork toward risk for PE pathogenesis. This overlap at the gene regulatory network level identifies possible shared therapeutic targets for future study.<\/jats:p>","DOI":"10.1093\/biolre\/ioad016","type":"journal-article","created":{"date-parts":[[2023,2,4]],"date-time":"2023-02-04T07:04:30Z","timestamp":1675494270000},"page":"659-670","source":"Crossref","is-referenced-by-count":4,"title":["Spatially constrained gene regulation identifies key genetic contributions of preeclampsia, hypertension, and proteinuria"],"prefix":"10.1093","volume":"108","author":[{"given":"Genevieve","family":"Boom","sequence":"first","affiliation":[{"name":"Liggins Institute, The University of Auckland , Auckland , New Zealand"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Justin M","family":"O\u2019Sullivan","sequence":"additional","affiliation":[{"name":"Liggins Institute, The University of Auckland , Auckland , New Zealand"},{"name":"The Maurice Wilkins Centre, The University of Auckland , Auckland , New 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