{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,24]],"date-time":"2026-08-24T16:19:48Z","timestamp":1787588388196,"version":"build-2736575974"},"reference-count":63,"publisher":"Wiley","license":[{"start":{"date-parts":[[2026,8,24]],"date-time":"2026-08-24T00:00:00Z","timestamp":1787529600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2026,8,24]],"date-time":"2026-08-24T00:00:00Z","timestamp":1787529600000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"content-domain":{"domain":["advanced.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Advanced Science"],"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:p>\n                    Our previous genome\u2010wide screening has linked\n                    <jats:italic>THSD7A<\/jats:italic>\n                    (thrombospondin type 1 domain containing 7A) gene to human coronary artery disease (CAD). How\n                    <jats:italic>THSD7A<\/jats:italic>\n                    contributes to atherosclerosis, however, remains unclear. In this study, we show THSD7A is increased in human carotid arteries and mouse atherosclerotic plaques. In apolipoprotein E knockout (\n                    <jats:italic>\n                      ApoE\n                      <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    <\/jats:italic>\n                    ) mice, the overexpression of\n                    <jats:italic>THSD7A<\/jats:italic>\n                    increases monocyte\u2010endothelial adhesion and macrophage infiltration, exacerbating atherosclerotic lesions, whereas\n                    <jats:italic>Thsd7A<\/jats:italic>\n                    knockout (\n                    <jats:italic>\n                      Thsd7A\n                      <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    <\/jats:italic>\n                    ) attenuates these phenotypic changes. Integrated single\u2010cell and bulk transcriptomic profiles demonstrate that\n                    <jats:italic>THSD7A<\/jats:italic>\n                    activates\n                    <jats:italic>IL1A<\/jats:italic>\n                    (Interleukin 1 alpha) signaling, augmenting endothelial inflammation. Mechanistically, THSD7A binds to integrin \u03b1v\u03b23, and such binding activates ERK (Extracellular signal\u2010regulated kinase) and augments\n                    <jats:italic>IL1A<\/jats:italic>\n                    \u2010associated proinflammatory signaling. Notably,\n                    <jats:italic>IL1A<\/jats:italic>\n                    serves as a transcriptional target of\n                    <jats:italic>CEBPD<\/jats:italic>\n                    (CCAAT\/enhancer\u2010binding protein delta), and\n                    <jats:italic>CEBPD<\/jats:italic>\n                    knockdown rescues\n                    <jats:italic>THSD7A\u2010<\/jats:italic>\n                    mediated endothelial inflammation. These findings establish\n                    <jats:italic>THSD7A<\/jats:italic>\n                    as a novel and critical mediator in the regulation of the\n                    <jats:italic>\u03b1v\u03b23\/CEBPD\/IL1A<\/jats:italic>\n                    axis that controls endothelial inflammatory responses associated with atherosclerosis and demonstrate the importance of\n                    <jats:italic>CEBPD<\/jats:italic>\n                    as a downstream molecule in mediating\n                    <jats:italic>THSD7A<\/jats:italic>\n                    \u2010associated signaling. This study positions\n                    <jats:italic>THSD7A<\/jats:italic>\n                    as both a genetic marker and a potential therapeutic target.\n                  <\/jats:p>","DOI":"10.1002\/advs.77422","type":"journal-article","created":{"date-parts":[[2026,8,24]],"date-time":"2026-08-24T15:20:35Z","timestamp":1787584835000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["<i>THSD7A<\/i>\n                    Exacerbates Atherosclerosis via Activation of Signaling Axis\n                    <i>\u03b1v\u03b23\/CEBPD\/IL1A<\/i>"],"prefix":"10.1002","author":[{"ORCID":"https:\/\/orcid.org\/0009-0006-6527-8945","authenticated-orcid":false,"given":"Jiankun","family":"Liu","sequence":"first","affiliation":[{"name":"Aging and Vascular Diseases Human Aging Research Institute and School of Life Science Nanchang University Jiangxi Key Laboratory of Aging and Diseases  Nanchang 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University Jiangxi Key Laboratory of Aging and Diseases  Nanchang China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yuanyuan","family":"Li","sequence":"additional","affiliation":[{"name":"Aging and Vascular Diseases Human Aging Research Institute and School of Life Science Nanchang University Jiangxi Key Laboratory of Aging and Diseases  Nanchang China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Bingbing","family":"Zhou","sequence":"additional","affiliation":[{"name":"Aging and Vascular Diseases Human Aging Research Institute and School of Life Science Nanchang University Jiangxi Key Laboratory of Aging and Diseases  Nanchang China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yangyi","family":"Zheng","sequence":"additional","affiliation":[{"name":"Aging and Vascular Diseases Human Aging Research Institute and School of Life Science Nanchang University Jiangxi Key Laboratory of Aging and Diseases  Nanchang 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