{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,18]],"date-time":"2026-05-18T07:06:55Z","timestamp":1779088015384,"version":"3.51.4"},"reference-count":6,"publisher":"Springer Science and Business Media LLC","issue":"11","license":[{"start":{"date-parts":[[2019,10,17]],"date-time":"2019-10-17T00:00:00Z","timestamp":1571270400000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2019,10,17]],"date-time":"2019-10-17T00:00:00Z","timestamp":1571270400000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["link.springer.com"],"crossmark-restriction":false},"short-container-title":["EMBO Mol Med"],"published-print":{"date-parts":[[2019,11,7]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>\n                    Heart failure entails the inability of the heart to pump blood to vital organs. One of the main risk factors for heart failure is the development of pathological hypertrophy. In this issue of\n                    <jats:italic>EMBO Molecular Medicine<\/jats:italic>\n                    , Li and coworkers show that NCoR1, a co\u2010repressor of transcription factors, inhibits the transcriptional activity of MEF2 by stabilizing its complex with class II HDACs. By this mechanism, NCoR1 was identified as potent inhibitor of pathological cardiac hypertrophy and dysfunction.\n                  <\/jats:p>","DOI":"10.15252\/emmm.201911297","type":"journal-article","created":{"date-parts":[[2019,10,17]],"date-time":"2019-10-17T05:48:43Z","timestamp":1571291323000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":4,"title":["Targeting cardiac hypertrophy through a nuclear co\u2010repressor"],"prefix":"10.1038","volume":"11","author":[{"given":"Andrea","family":"Grund","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-1541-3030","authenticated-orcid":false,"given":"Joerg","family":"Heineke","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"297","published-online":{"date-parts":[[2019,10,17]]},"reference":[{"key":"BFEMMM201911297_CR1","doi-asserted-by":"crossref","first-page":"15","DOI":"10.1161\/01.RES.0000197782.21444.8f","volume":"98","author":"J Backs","year":"2006","unstructured":"Backs J, Olson EN (2006) Control of cardiac growth by histone acetylation\/deacetylation. 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