{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,27]],"date-time":"2026-06-27T07:27:20Z","timestamp":1782545240400,"version":"3.54.5"},"reference-count":14,"publisher":"American Society for Clinical Investigation","issue":"15","license":[{"start":{"date-parts":[[2024,8,1]],"date-time":"2024-08-01T00:00:00Z","timestamp":1722470400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2024,8,1]]},"abstract":"<jats:p>\n                    Cerebral arteriovenous malformations represent the most common form of vascular malformations and can cause recurrent bleeding and hemorrhagic stroke. The current issue of the\n                    <jats:italic>JCI<\/jats:italic>\n                    features an article by Zhao et al. describing a mouse model of cerebral arteriovenous malformations. Endothelial cells lacking matrix Gla protein, a BMP inhibitor, underwent epigenetic changes characteristic of an endothelial-to-mesenchymal fate transition. The authors uncovered a two-step process for this transition controlled by the epigenetic regulator histone deacetylase 2 (HDAC2), which controls endothelial cell differentiation, and by enhancer of zeste homolog 1 (EZH1), which suppressed mesenchymal fate. This discovery provides a promising entry point for preventive pharmacological interventions.\n                  <\/jats:p>","DOI":"10.1172\/jci182904","type":"journal-article","created":{"date-parts":[[2024,7,31]],"date-time":"2024-07-31T14:05:16Z","timestamp":1722434716000},"source":"Crossref","is-referenced-by-count":5,"title":["Epigenetics enters the stage in vascular malformations"],"prefix":"10.1172","volume":"134","author":[{"given":"Salim","family":"Abdelilah-Seyfried","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"232","published-online":{"date-parts":[[2024,8,1]]},"reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1038\/ng0696-189"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1038\/ng1294-345"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1016\/S0140-6736(04)15732-2"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1172\/JCI176758"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1161\/CIRCRESAHA.120.317439"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1172\/JCI57567"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1183\/09031936.00114714"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.3389\/fcell.2021.642136"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1016\/j.cell.2016.06.028"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1101\/cshperspect.a018713"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1101\/gad.2019811"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1016\/j.ydbio.2017.02.017"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1016\/j.molcel.2008.10.016"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1038\/nature12207"}],"container-title":["Journal of Clinical Investigation"],"original-title":[],"language":"en","link":[{"URL":"https:\/\/www.jci.org\/articles\/view\/182904\/files\/pdf","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2026,5,19]],"date-time":"2026-05-19T23:27:03Z","timestamp":1779233223000},"score":1,"resource":{"primary":{"URL":"https:\/\/www.jci.org\/articles\/view\/182904"}},"subtitle":[],"short-title":[],"issued":{"date-parts":[[2024,8,1]]},"references-count":14,"journal-issue":{"issue":"15","published-online":{"date-parts":[[2024,6,17]]},"published-print":{"date-parts":[[2024,8,1]]}},"alternative-id":["10.1172\/JCI182904"],"URL":"https:\/\/doi.org\/10.1172\/jci182904","relation":{},"ISSN":["1558-8238"],"issn-type":[{"value":"1558-8238","type":"electronic"}],"subject":[],"published":{"date-parts":[[2024,8,1]]},"article-number":"e182904"}}