{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,22]],"date-time":"2026-07-22T05:06:57Z","timestamp":1784696817477,"version":"3.55.0"},"reference-count":34,"publisher":"SAGE Publications","issue":"8","license":[{"start":{"date-parts":[[2025,10,5]],"date-time":"2025-10-05T00:00:00Z","timestamp":1759622400000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.sagepub.com\/page\/policies\/text-and-data-mining-license"}],"content-domain":{"domain":["journals.sagepub.com"],"crossmark-restriction":true},"short-container-title":["Angiology"],"published-print":{"date-parts":[[2026,9]]},"abstract":"<jats:p>\n                    This study investigated SOX18\u2019s role in calcific aortic valve disease (CAVD). Aortic valve specimens from 67 patients undergoing valve replacement were stratified into control (n\u2009=\u200918), mild (n\u2009=\u200920), and severe calcification (n\u2009=\u200929) groups based on Alizarin Red staining. Immunohistochemistry revealed SOX18 expression localized to valve interstitial cells (VICs), with significantly higher levels in calcified versus control valves (\n                    <jats:italic toggle=\"yes\">P<\/jats:italic>\n                    \u2009&lt;\u2009.001). Elevated SOX18 was particularly associated with the inflammatory factors CD68 and Nuclear Factor-kappa B (NF-\u03baB) p65, suggesting a potential link between SOX18, inflammation and CAVD progression. These findings highlight SOX18 as a possible mediator in valvular calcification.\n                  <\/jats:p>","DOI":"10.1177\/00033197251376086","type":"journal-article","created":{"date-parts":[[2025,10,5]],"date-time":"2025-10-05T10:26:18Z","timestamp":1759659978000},"page":"981-987","update-policy":"https:\/\/doi.org\/10.1177\/sage-journals-update-policy","source":"Crossref","is-referenced-by-count":0,"title":["SRY-Box Transcription Factor 18 Links Inflammation to Calcific Aortic Valve Progression via CD68 and NF-\u03baB p65"],"prefix":"10.1177","volume":"77","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-6649-0415","authenticated-orcid":false,"given":"Li","family":"Ke-xin","sequence":"first","affiliation":[{"name":"Pathology Department, The Fifth Affiliated Hospital of Sun Yat-sen University, Zhuhai, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-7422-3811","authenticated-orcid":false,"given":"Luo","family":"Yi-chen","sequence":"additional","affiliation":[{"name":"Pathology Department, The Fifth Affiliated Hospital of Sun Yat-sen University, Zhuhai, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-3320-8348","authenticated-orcid":false,"given":"Huang","family":"Hao","sequence":"additional","affiliation":[{"name":"Pathology Department, The Fifth Affiliated Hospital of Sun Yat-sen University, Zhuhai, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0009-0003-5078-0412","authenticated-orcid":false,"given":"Chen","family":"Yan-ting","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"179","published-online":{"date-parts":[[2025,10,5]]},"reference":[{"key":"e_1_3_3_2_2","doi-asserted-by":"publisher","DOI":"10.1161\/01.CIR.90.2.844"},{"key":"e_1_3_3_3_2","doi-asserted-by":"publisher","DOI":"10.1038\/s41569-023-00845-7"},{"key":"e_1_3_3_4_2","doi-asserted-by":"publisher","DOI":"10.15698\/mic2023.02.791"},{"issue":"3","key":"e_1_3_3_5_2","first-page":"31","article-title":"Lipoprotein(a) gene polymorphism increases a risk factor for aortic valve calcification","volume":"6","author":"Ozkan U","year":"2019","unstructured":"Ozkan U, Ozcelik F, Yildiz M, Budak M. Lipoprotein(a) gene polymorphism increases a risk factor for aortic valve calcification. J Cardiovasc Dev Dis. 2019;6(3):31.","journal-title":"J Cardiovasc Dev Dis"},{"key":"e_1_3_3_6_2","doi-asserted-by":"publisher","DOI":"10.1038\/nrdp.2016.6"},{"issue":"5","key":"e_1_3_3_7_2","article-title":"2020 ACC\/AHA guideline for the management of patients with valvular heart disease: a report of the American College of Cardiology\/American Heart Association Joint Committee on Clinical Practice Guidelines","volume":"143","author":"Otto CM","year":"2021","unstructured":"Otto CM, Nishimura RA, Bonow RO, et al. 2020 ACC\/AHA guideline for the management of patients with valvular heart disease: a report of the American College of Cardiology\/American Heart Association Joint Committee on Clinical Practice Guidelines. Circulation. 2021;143(5):e35-e71.","journal-title":"Circulation"},{"key":"e_1_3_3_8_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.ihj.2015.09.010"},{"key":"e_1_3_3_9_2","doi-asserted-by":"publisher","DOI":"10.1038\/346245a0"},{"key":"e_1_3_3_10_2","doi-asserted-by":"publisher","DOI":"10.1038\/348450a0"},{"key":"e_1_3_3_11_2","doi-asserted-by":"publisher","DOI":"10.1242\/dev.091793"},{"key":"e_1_3_3_12_2","doi-asserted-by":"publisher","DOI":"10.1016\/S1050-1738(01)00131-1"},{"key":"e_1_3_3_13_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.bbrc.2007.06.093"},{"key":"e_1_3_3_14_2","doi-asserted-by":"publisher","DOI":"10.1182\/blood-2013-04-495432"},{"key":"e_1_3_3_15_2","doi-asserted-by":"publisher","DOI":"10.1161\/01.ATV.0000187464.81959.23"},{"key":"e_1_3_3_16_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.yjmcc.2024.11.015"},{"key":"e_1_3_3_17_2","doi-asserted-by":"publisher","DOI":"10.1038\/s41467-022-31815-1"},{"key":"e_1_3_3_18_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.ihj.2015.07.033"},{"key":"e_1_3_3_19_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.yjmcc.2019.05.016"},{"key":"e_1_3_3_20_2","doi-asserted-by":"publisher","DOI":"10.1242\/dev.183020"},{"issue":"2","key":"e_1_3_3_21_2","first-page":"744","article-title":"HDAC I inhibitor regulates RUNX2 transactivation through canonical and non-canonical Wnt signaling in aortic valvular interstitial cells","volume":"11","author":"Li SJ","year":"2019","unstructured":"Li SJ, Kao YH, Chung CC, Cheng WL, Chen YJ. HDAC I inhibitor regulates RUNX2 transactivation through canonical and non-canonical Wnt signaling in aortic valvular interstitial cells. Am J Transl Res. 2019;11(2):744-754.","journal-title":"Am J Transl Res"},{"issue":"3","key":"e_1_3_3_22_2","doi-asserted-by":"crossref","DOI":"10.1096\/fj.202002013RR","article-title":"Tumor necrosis factor-\u03b1 promotes and exacerbates calcification in heart valve myofibroblast populations","volume":"35","author":"Gonzalez Rodriguez A","year":"2021","unstructured":"Gonzalez Rodriguez A, Schroeder ME, Grim JC, et al. Tumor necrosis factor-\u03b1 promotes and exacerbates calcification in heart valve myofibroblast populations. FASEB J. 2021;35(3):e21382.","journal-title":"FASEB J"},{"issue":"7","key":"e_1_3_3_23_2","first-page":"3329","article-title":"Inorganic phosphate-osteogenic induction medium promotes osteogenic differentiation of valvular interstitial cells via the BMP-2\/Smad1\/5\/9 and RhoA\/ROCK-1 signaling pathways","volume":"12","author":"Lu C","year":"2020","unstructured":"Lu C, Dong X, Yu WP, et al. Inorganic phosphate-osteogenic induction medium promotes osteogenic differentiation of valvular interstitial cells via the BMP-2\/Smad1\/5\/9 and RhoA\/ROCK-1 signaling pathways. Am J Transl Res. 2020;12(7):3329-3345.","journal-title":"Am J Transl Res"},{"key":"e_1_3_3_24_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.ejcb.2015.08.002"},{"key":"e_1_3_3_25_2","doi-asserted-by":"publisher","DOI":"10.1111\/j.1600-0854.2009.00937.x"},{"key":"e_1_3_3_26_2","doi-asserted-by":"publisher","DOI":"10.3389\/fphys.2018.00201"},{"key":"e_1_3_3_27_2","doi-asserted-by":"publisher","DOI":"10.1155\/2022\/2676114"},{"key":"e_1_3_3_28_2","doi-asserted-by":"publisher","DOI":"10.3389\/fcvm.2022.783543"},{"key":"e_1_3_3_29_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.jbc.2022.101887"},{"key":"e_1_3_3_30_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.molcel.2014.08.024"},{"key":"e_1_3_3_31_2","doi-asserted-by":"publisher","DOI":"10.1155\/2015\/851945"},{"key":"e_1_3_3_32_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.intimp.2021.107746"},{"key":"e_1_3_3_33_2","doi-asserted-by":"publisher","DOI":"10.1080\/02770903.2020.1771727"},{"key":"e_1_3_3_34_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.semcdb.2016.07.021"},{"key":"e_1_3_3_35_2","doi-asserted-by":"publisher","DOI":"10.1242\/jcs.03081"}],"container-title":["Angiology"],"original-title":[],"language":"en","link":[{"URL":"https:\/\/journals.sagepub.com\/doi\/pdf\/10.1177\/00033197251376086","content-type":"application\/pdf","content-version":"vor","intended-application":"text-mining"},{"URL":"https:\/\/journals.sagepub.com\/doi\/full-xml\/10.1177\/00033197251376086","content-type":"application\/xml","content-version":"vor","intended-application":"text-mining"},{"URL":"https:\/\/journals.sagepub.com\/doi\/pdf\/10.1177\/00033197251376086","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2026,7,22]],"date-time":"2026-07-22T04:50:24Z","timestamp":1784695824000},"score":1,"resource":{"primary":{"URL":"https:\/\/journals.sagepub.com\/doi\/10.1177\/00033197251376086"}},"subtitle":[],"short-title":[],"issued":{"date-parts":[[2025,10,5]]},"references-count":34,"journal-issue":{"issue":"8","published-print":{"date-parts":[[2026,9]]}},"alternative-id":["10.1177\/00033197251376086"],"URL":"https:\/\/doi.org\/10.1177\/00033197251376086","relation":{},"ISSN":["0003-3197","1940-1574"],"issn-type":[{"value":"0003-3197","type":"print"},{"value":"1940-1574","type":"electronic"}],"subject":[],"published":{"date-parts":[[2025,10,5]]}}}