{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,2,2]],"date-time":"2026-02-02T18:38:45Z","timestamp":1770057525720,"version":"3.49.0"},"reference-count":20,"publisher":"Oxford University Press (OUP)","issue":"4","license":[{"start":{"date-parts":[[2007,3,24]],"date-time":"2007-03-24T00:00:00Z","timestamp":1174694400000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/pages\/standard-publication-reuse-rights"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2007,4,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>Left ventricular (LV) hypertrophy (LVH) is an adaptive response to hemodynamic overload, but also contributes to the pathogenesis of heart failure. LVH can be concentric (cLVH) but subsequent dilatation and progression to eccentric hypertrophy (eLVH) may lead to global pump failure. Recently, several endogenous molecular inhibitors of hypertrophy have been identified. Using real-time PCR, we compared the myocardial mRNA expression of these inhibitors in pressure-overload induced cLVH (severe aortic stenosis) and in volume overload-induced eLVH (severe mitral regurgitation) in patients, and during the progression from cLVH to eLVH in pressure overload in rat. Each of these genes showed a unique temporal expression profile. Strikingly, except for SOCS-3, changes in gene expression of these negative regulators in rat cLVH and eLVH vs sham were recapitulated in human cLVH and eLVH. In particular, VDUP-1 and MCIP-1 were high in cLVH but expression levels were normal in eLVH, both in rat and human. These data indicate that during the progression of LVH, both in pressure and volume overload, expression levels of endogenous inhibitors of hypertrophy are modified and that these changes may have pathophysiological significance. In particular, MCIP-1 (the endogenous calcineurin inhibitor) and VDUP-1 (the endogenous inhibitor of thioredoxin) are potential molecular switches in the progression of LV hypertrophy.<\/jats:p>","DOI":"10.1016\/j.ejheart.2006.10.002","type":"journal-article","created":{"date-parts":[[2006,11,29]],"date-time":"2006-11-29T17:25:15Z","timestamp":1164821115000},"page":"352-356","source":"Crossref","is-referenced-by-count":12,"title":["Endogenous Inhibitors of Hypertrophy in Concentric Versus Eccentric Hypertrophy"],"prefix":"10.1093","volume":"9","author":[{"given":"Katrien","family":"Lemmens","sequence":"first","affiliation":[{"name":"Laboratory of Physiology, University of Antwerp , Groenenborgerlaan 171, 2020, Antwerp ,","place":["Belgium"]}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Vincent F.M.","family":"Segers","sequence":"additional","affiliation":[{"name":"Laboratory of Physiology, University of Antwerp , Groenenborgerlaan 171, 2020, Antwerp ,","place":["Belgium"]}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Marc","family":"Demolder","sequence":"additional","affiliation":[{"name":"Laboratory of Physiology, University of Antwerp , Groenenborgerlaan 171, 2020, Antwerp ,","place":["Belgium"]}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Maria","family":"Michiels","sequence":"additional","affiliation":[{"name":"Laboratory of Physiology, University of Antwerp , Groenenborgerlaan 171, 2020, Antwerp ,","place":["Belgium"]}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Philip","family":"Van Cauwelaert","sequence":"additional","affiliation":[{"name":"Department of Cardiac Surgery, Middelheim Hospital , Antwerp ,","place":["Belgium"]}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Gilles W.","family":"De Keulenaer","sequence":"additional","affiliation":[{"name":"Laboratory of Physiology, University of Antwerp , Groenenborgerlaan 171, 2020, Antwerp ,","place":["Belgium"]}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"286","published-online":{"date-parts":[[2007,3,24]]},"reference":[{"key":"2026020203465554200_ejhf2006-10-002-bib-0001","doi-asserted-by":"crossref","first-page":"1580","DOI":"10.1161\/01.CIR.0000120390.68287.BB","article-title":"Hypertrophy of the heart: a new therapeutic target?","volume":"109","author":"Frey","year":"2004","journal-title":"Circulation"},{"key":"2026020203465554200_ejhf2006-10-002-bib-0002","doi-asserted-by":"crossref","first-page":"936","DOI":"10.1161\/CIRCULATIONAHA.105.558734","article-title":"The transition from hypertrophy to failure: how certain are we?","volume":"112","author":"Drazner","year":"2005","journal-title":"Circulation"},{"key":"2026020203465554200_ejhf2006-10-002-bib-0003","doi-asserted-by":"crossref","first-page":"1459","DOI":"10.1161\/01.CIR.103.10.1459","article-title":"Regulation of cardiomyocyte mechanotransduction by the cardiac cycle","volume":"103","author":"Yamamoto","year":"2001","journal-title":"Circulation"},{"key":"2026020203465554200_ejhf2006-10-002-bib-0004","doi-asserted-by":"crossref","first-page":"185","DOI":"10.1016\/j.tcm.2005.05.009","article-title":"Physiologic growth and pathologic genes in cardiac development and cardiomyopathy","volume":"15","author":"Dorn","year":"2005","journal-title":"Trends Cardiovasc Med"},{"key":"2026020203465554200_ejhf2006-10-002-bib-0005","doi-asserted-by":"crossref","first-page":"849","DOI":"10.1172\/JCI0215380","article-title":"Mixed signals in heart failure: cancer rules","volume":"109","author":"Hoshijima","year":"2002","journal-title":"J Clin Invest"},{"key":"2026020203465554200_ejhf2006-10-002-bib-0006","doi-asserted-by":"crossref","first-page":"1127","DOI":"10.1161\/01.RES.84.10.1127","article-title":"Mechanical stretch activates the JAK\/STAT pathway in rat cardiomyocytes","volume":"84","author":"Pan","year":"1999","journal-title":"Circ Res"},{"key":"2026020203465554200_ejhf2006-10-002-bib-0007","doi-asserted-by":"crossref","first-page":"26496","DOI":"10.1074\/jbc.M202133200","article-title":"Vitamin D(3)-up-regulated protein-1 is a stress-responsive gene that regulates cardiomyocyte viability through interaction with thioredoxin","volume":"277","author":"Wang","year":"2002","journal-title":"J Biol Chem"},{"key":"2026020203465554200_ejhf2006-10-002-bib-0008","doi-asserted-by":"crossref","first-page":"690","DOI":"10.1161\/01.RES.0000012922.40318.05","article-title":"Identification of IEX-1 as a biomechanically controlled nuclear factor-kappaB target gene that inhibits cardiomyocyte hypertrophy","volume":"90","author":"De Keulenaer","year":"2002","journal-title":"Circ Res"},{"key":"2026020203465554200_ejhf2006-10-002-bib-0009","doi-asserted-by":"crossref","first-page":"500","DOI":"10.1016\/j.cardiores.2004.03.015","article-title":"Negative regulators of cardiac hypertrophy","volume":"63","author":"Hardt","year":"2004","journal-title":"Cardiovasc Res"},{"key":"2026020203465554200_ejhf2006-10-002-bib-0010","doi-asserted-by":"crossref","first-page":"1459","DOI":"10.1172\/JCI13939","article-title":"Suppressor of cytokine signaling-3 is a biomechanical stress-inducible gene that suppresses gp130-mediated cardiac myocyte hypertrophy and survival pathways","volume":"108","author":"Yasukawa","year":"2001","journal-title":"J Clin Invest"},{"key":"2026020203465554200_ejhf2006-10-002-bib-0011","doi-asserted-by":"crossref","first-page":"H533","DOI":"10.1152\/ajpheart.00002.2002","article-title":"Direct biomechanical induction of endogenous calcineurin inhibitor Down Syndrome Critical Region-1 in cardiac myocytes","volume":"283","author":"Wang","year":"2002","journal-title":"Am J Physiol Heart Circ Physiol"},{"key":"2026020203465554200_ejhf2006-10-002-bib-0012","doi-asserted-by":"crossref","first-page":"88","DOI":"10.1161\/01.RES.88.1.88","article-title":"The dual-specificity phosphatase MKP-1 limits the cardiac hypertrophic response in vitro and in vivo","volume":"88","author":"Bueno","year":"2001","journal-title":"Circ Res"},{"key":"2026020203465554200_ejhf2006-10-002-bib-0013","doi-asserted-by":"crossref","first-page":"3328","DOI":"10.1073\/pnas.041614798","article-title":"Myocyte-enriched calcineurin-interacting protein, MCIP1, inhibits cardiac hypertrophy in vivo","volume":"98","author":"Rothermel","year":"2001","journal-title":"Proc Natl Acad Sci U S A"},{"key":"2026020203465554200_ejhf2006-10-002-bib-0014","doi-asserted-by":"crossref","first-page":"585","DOI":"10.1002\/(SICI)1097-010X(20000501)286:6<585::AID-JEZ5>3.0.CO;2-Z","article-title":"Calculation of volumes and systolic indices of heart ventricle from Halobatrachus didactylus: echocardiographic noninvasive method","volume":"286","author":"Coucelo","year":"2000","journal-title":"J Exp Zool"},{"key":"2026020203465554200_ejhf2006-10-002-bib-0015","doi-asserted-by":"crossref","first-page":"450","DOI":"10.1016\/0002-9149(86)90771-X","article-title":"Echocardiographic assessment of left ventricular hypertrophy: comparison to necropsy findings","volume":"57","author":"Devereux","year":"1986","journal-title":"Am J Cardiol"},{"key":"2026020203465554200_ejhf2006-10-002-bib-0016","doi-asserted-by":"crossref","first-page":"7","DOI":"10.1016\/0002-9149(76)90491-4","article-title":"Problems in echocardiographic volume determinations: echocardiographic-angiographic correlations in the presence of absence of asynergy","volume":"37","author":"Teichholz","year":"1976","journal-title":"Am J Cardiol"},{"key":"2026020203465554200_ejhf2006-10-002-bib-0017","doi-asserted-by":"crossref","first-page":"491","DOI":"10.1291\/hypres.25.491","article-title":"Inhibitory molecules in signal transduction pathways of cardiac hypertrophy","volume":"25","author":"Takano","year":"2002","journal-title":"Hypertens Res"},{"key":"2026020203465554200_ejhf2006-10-002-bib-0018","doi-asserted-by":"crossref","first-page":"18","DOI":"10.1152\/physiolgenomics.00061.2005","article-title":"Differential activation of stress-response signaling in load-induced cardiac hypertrophy and failure","volume":"23","author":"Rothermel","year":"2005","journal-title":"Physiol Genomics"},{"key":"2026020203465554200_ejhf2006-10-002-bib-0019","doi-asserted-by":"crossref","first-page":"670","DOI":"10.1161\/01.CIR.103.5.670","article-title":"Differential activation of signal transduction pathways in human hearts with hypertrophy versus advanced heart failure","volume":"103","author":"Haq","year":"2001","journal-title":"Circulation"},{"key":"2026020203465554200_ejhf2006-10-002-bib-0020","doi-asserted-by":"crossref","first-page":"2581","DOI":"10.1161\/01.CIR.0000129771.32215.44","article-title":"Thioredoxin-interacting protein controls cardiac hypertrophy through regulation of thioredoxin activity","volume":"109","author":"Yoshioka","year":"2004","journal-title":"Circulation"}],"container-title":["European Journal of Heart Failure"],"original-title":[],"language":"en","link":[{"URL":"https:\/\/api.wiley.com\/onlinelibrary\/tdm\/v1\/articles\/10.1016%2Fj.ejheart.2006.10.002","content-type":"unspecified","content-version":"vor","intended-application":"text-mining"},{"URL":"https:\/\/academic.oup.com\/eurjhf\/article-pdf\/9\/4\/352\/66615303\/eurjhf_9_4_352.pdf","content-type":"application\/pdf","content-version":"vor","intended-application":"syndication"},{"URL":"https:\/\/academic.oup.com\/eurjhf\/article-pdf\/9\/4\/352\/66615303\/eurjhf_9_4_352.pdf","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2026,2,2]],"date-time":"2026-02-02T08:47:03Z","timestamp":1770022023000},"score":1,"resource":{"primary":{"URL":"https:\/\/academic.oup.com\/eurjhf\/article\/9\/4\/352\/8443619"}},"subtitle":[],"short-title":[],"issued":{"date-parts":[[2007,3,24]]},"references-count":20,"journal-issue":{"issue":"4","published-online":{"date-parts":[[2007,3,24]]},"published-print":{"date-parts":[[2007,4,1]]}},"URL":"https:\/\/doi.org\/10.1016\/j.ejheart.2006.10.002","relation":{},"ISSN":["1388-9842","1879-0844"],"issn-type":[{"value":"1388-9842","type":"print"},{"value":"1879-0844","type":"electronic"}],"subject":[],"published-other":{"date-parts":[[2007,4]]},"published":{"date-parts":[[2007,3,24]]}}}