{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,2,26]],"date-time":"2026-02-26T20:18:09Z","timestamp":1772137089045,"version":"3.50.1"},"reference-count":75,"publisher":"Portland Press Ltd.","issue":"11","license":[{"start":{"date-parts":[[2025,6,3]],"date-time":"2025-06-03T00:00:00Z","timestamp":1748908800000},"content-version":"vor","delay-in-days":2,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["portlandpress.com"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2025,6,11]]},"abstract":"<jats:p>In United States, six million individuals with sub-Saharan ancestry carry two APOL1 high-risk variants, which increase the risk for kidney diseases. Whether APOL1 high-risk variants increase other diseases under dyslipidemia remains unclear and requires further investigation. We characterized a mouse model to investigate the role of APOL1 in dyslipidemia and cardiovascular diseases (CVDs). Transgenic mice carrying APOL1 (G0 and G1 variants) on bacterial artificial chromosomes (BAC\/APOL1 mice) were crossed with the apolipoprotein-E knock-out (ApoE-KO) dyslipidemia and atherosclerosis mouse model. The compound transgenic mice were evaluated for the impact of APOL1 on systemic phenotypes. ApoE-KO mice carrying APOL1-G0 and APOL1-G1 did not show differences in the extent of atherosclerotic lesions or aortic calcification, as evaluated by Sudan IV staining and radiographic examination, respectively. However, ~20% of ApoE-KO; BAC\/APOL1-G1 mice developed hydrocephalus and required euthanasia. The hydrocephalus was communicating and likely was due to excess cerebrospinal fluid produced by the choroid plexus, where epithelial cells expressed APOL1. Single-nuclear RNA-seq of choroid plexus identified solute transporter up-regulation and mTORC2 pathway activation in APOL1-G1-expressing epithelial cells. Further, in the All of Us cohort, we found higher hydrocephalus prevalence among individuals with the APOL1-G1 variant in both recessive and dominant models, supporting the mouse findings. While APOL1-G1 expression in ApoE-KO mice did not worsen CVD phenotypes, we uncovered hydrocephalus as a novel APOL1 risk allele-mediated phenotype. These findings extend the spectrum of APOL1-associated pathologies.<\/jats:p>","DOI":"10.1042\/cs20255324","type":"journal-article","created":{"date-parts":[[2025,6,3]],"date-time":"2025-06-03T07:19:22Z","timestamp":1748935162000},"page":"559-575","update-policy":"https:\/\/doi.org\/10.1042\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Apolipoprotein-L1 G1 variant contributes to hydrocephalus but not to atherosclerosis in apolipoprotein-E knock-out mice"],"prefix":"10.1042","volume":"139","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-2049-7347","authenticated-orcid":false,"given":"Teruhiko","family":"Yoshida","sequence":"first","affiliation":[{"name":"1National Institute of Diabetes and Digestive and Kidney Diseases, NIH, Bethesda, MD, U.S.A"},{"name":"2Graduate School of Medicine, The University of Tokyo, Tokyo, 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