{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,30]],"date-time":"2026-07-30T22:19:02Z","timestamp":1785449942500,"version":"3.56.0"},"reference-count":16,"publisher":"Springer Science and Business Media LLC","issue":"4","license":[{"start":{"date-parts":[[2014,3,12]],"date-time":"2014-03-12T00:00:00Z","timestamp":1394582400000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2014,3,12]],"date-time":"2014-03-12T00:00:00Z","timestamp":1394582400000},"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":[[2014,4,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>\n                    The heart has been recognized as an endocrine organ for over 30\u00a0years (de Bold, 2011); however, little is known about how the heart communicates with other organs in the body, and even less is known about this process in the diseased heart. In this issue of\n                    <jats:italic>EMBO Molecular Medicine<\/jats:italic>\n                    , Magida and Leinwand (2014) introduce the concept that a primary genetic defect in the heart results in aberrant hepatic lipid metabolism, which consequently exacerbates hypertrophic cardiomyopathy (HCM). This study provides evidence in support of the hypothesis that crosstalk occurs between the heart and liver, and that this becomes disrupted in the diseased state.\n                  <\/jats:p>","DOI":"10.1002\/emmm.201303800","type":"journal-article","created":{"date-parts":[[2014,3,19]],"date-time":"2014-03-19T14:38:30Z","timestamp":1395239910000},"page":"436-438","update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":29,"title":["The heart\u2010liver metabolic axis: defective communication exacerbates disease"],"prefix":"10.1038","volume":"6","author":[{"given":"Kedryn K","family":"Baskin","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Angie L","family":"Bookout","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Eric N","family":"Olson","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2014,3,12]]},"reference":[{"key":"BFEMMM201303800_CR1","doi-asserted-by":"crossref","first-page":"1190","DOI":"10.1093\/eurheartj\/ehr453","volume":"33","author":"LS Bhatia","year":"2012","unstructured":"Bhatia LS, Curzen NP, Calder PC, Byrne CD (2012) Non\u2010alcoholic fatty liver disease: a new and important cardiovascular risk factor? 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