{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,23]],"date-time":"2026-10-23T20:33:45Z","timestamp":1792787625220,"version":"4.5.0"},"reference-count":27,"publisher":"American Society for Clinical Investigation","issue":"2","funder":[{"name":"NIH","award":["HL130113"],"award-info":[{"award-number":["HL130113"]}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2019,1,24]]},"abstract":"<jats:p>\n                    Patients with heterozygous missense mutations in the\n                    <jats:italic>ACTA2<\/jats:italic>\n                    or\n                    <jats:italic>MYH11<\/jats:italic>\n                    gene are known to exhibit thoracic aortic aneurysm and a risk of early-onset aortic dissection. However, less common phenotypes involving arterial obstruction are also observed, including coronary and cerebrovascular stenotic disease. Herein we implicate the HDAC9 complex in transcriptional silencing of contractile protein\u2013associated genes, known to undergo downregulation in stenotic lesions. Furthermore, neointimal formation was inhibited in HDAC9- or MALAT1-deficient mice with preservation of contractile protein expression. Pharmacologic targeting of the HDAC9 complex through either MALAT1 antisense oligonucleotides or inhibition of the methyltransferase EZH2 (catalytic mediator recruited by the HDAC9 complex) reduced neointimal formation. In conclusion, we report the implication of the HDAC9 complex in stenotic disease and demonstrate that pharmacologic therapy targeting epigenetic complexes can ameliorate arterial obstruction in an experimental system.\n                  <\/jats:p>","DOI":"10.1172\/jci.insight.124706","type":"journal-article","created":{"date-parts":[[2019,1,23]],"date-time":"2019-01-23T11:01:58Z","timestamp":1548241318000},"source":"Crossref","is-referenced-by-count":30,"title":["HDAC9 complex inhibition improves smooth muscle\u2013dependent stenotic vascular disease"],"prefix":"10.1172","volume":"4","author":[{"given":"Christian L.","family":"Lino Cardenas","sequence":"first","affiliation":[{"name":"Cardiovascular Research Center, Cardiology Division, Department of Medicine,"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Chase W.","family":"Kessinger","sequence":"additional","affiliation":[{"name":"Cardiovascular Research Center, Cardiology Division, Department of 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