{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,1]],"date-time":"2026-10-01T17:14:30Z","timestamp":1790874870591,"version":"4.1.0"},"reference-count":47,"publisher":"The Endocrine Society","issue":"1","license":[{"start":{"date-parts":[[2016,11,23]],"date-time":"2016-11-23T00:00:00Z","timestamp":1479859200000},"content-version":"vor","delay-in-days":327,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2016,1,1]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Global deficiency of 11\u03b2-hydroxysteroid dehydrogenase type 1 (11\u03b2-HSD1), an enzyme that regenerates glucocorticoids within cells, promotes angiogenesis, and reduces acute infarct expansion after myocardial infarction (MI), suggesting that 11\u03b2-HSD1 activity has an adverse influence on wound healing in the heart after MI. The present study investigated whether 11\u03b2-HSD1 deficiency could prevent the development of heart failure after MI and examined whether 11\u03b2-HSD1 deficiency in cardiomyocytes and vascular smooth muscle cells confers this protection. Male mice with global deficiency in 11\u03b2-HSD1, or with Hsd11b1 disruption in cardiac and vascular smooth muscle (via SM22\u03b1-Cre recombinase), underwent coronary artery ligation for induction of MI. Acute injury was equivalent in all groups. However, by 8 weeks after induction of MI, relative to C57Bl\/6 wild type, globally 11\u03b2-HSD1-deficient mice had reduced infarct size (34.7 \u00b1 2.1% left ventricle [LV] vs 44.0 \u00b1 3.3% LV, P = .02), improved function (ejection fraction, 33.5 \u00b1 2.5% vs 24.7 \u00b1 2.5%, P = .03) and reduced ventricular dilation (LV end-diastolic volume, 0.17 \u00b1 0.01 vs 0.21 \u00b1 0.01 mL, P = .01). This was accompanied by a reduction in hypertrophy, pulmonary edema, and in the expression of genes encoding atrial natriuretic peptide and \u03b2-myosin heavy chain. None of these outcomes, nor promotion of periinfarct angiogenesis during infarct repair, were recapitulated when 11\u03b2-HSD1 deficiency was restricted to cardiac and vascular smooth muscle. 11\u03b2-HSD1 expressed in cells other than cardiomyocytes or vascular smooth muscle limits angiogenesis and promotes infarct expansion with adverse ventricular remodeling after MI. Early pharmacological inhibition of 11\u03b2-HSD1 may offer a new therapeutic approach to prevent heart failure associated with ischemic heart disease.<\/jats:p>","DOI":"10.1210\/en.2015-1630","type":"journal-article","created":{"date-parts":[[2015,10,14]],"date-time":"2015-10-14T17:08:39Z","timestamp":1444842519000},"page":"346-357","source":"Crossref","is-referenced-by-count":34,"title":["Cardiomyocyte and Vascular Smooth Muscle-Independent 11\u03b2-Hydroxysteroid Dehydrogenase 1 Amplifies Infarct Expansion, Hypertrophy, and the Development of Heart Failure After Myocardial Infarction in Male Mice"],"prefix":"10.1210","volume":"157","author":[{"given":"Christopher I.","family":"White","sequence":"first","affiliation":[{"name":"British Heart Foundation\/University Centre for Cardiovascular Science (C.I.W., M.A.J., K.M., K.J.M., R.V.R., C.M.M., J.R.S., B.R.W., K.E.C., G.A.G.), Edinburgh EH16 4TJ, Scotland, United Kingdom"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Maurits A.","family":"Jansen","sequence":"first","affiliation":[{"name":"British Heart Foundation\/University Centre for Cardiovascular Science (C.I.W., M.A.J., K.M., K.J.M., R.V.R., C.M.M., J.R.S., B.R.W., K.E.C., G.A.G.), Edinburgh EH16 4TJ, Scotland, United Kingdom"},{"name":"Queens Medical Research Institute, and Edinburgh Preclinical Imaging (M.A.J., A.T., C.M.M.), College of Medicine and Veterinary Medicine, The University of Edinburgh, Edinburgh EH16 4TJ, Scotland, United Kingdom"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kieran","family":"McGregor","sequence":"first","affiliation":[{"name":"British Heart Foundation\/University Centre for Cardiovascular Science (C.I.W., M.A.J., K.M., K.J.M., R.V.R., C.M.M., J.R.S., B.R.W., K.E.C., G.A.G.), Edinburgh EH16 4TJ, Scotland, United Kingdom"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Katie 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Kingdom"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Carmel M.","family":"Moran","sequence":"first","affiliation":[{"name":"British Heart Foundation\/University Centre for Cardiovascular Science (C.I.W., M.A.J., K.M., K.J.M., R.V.R., C.M.M., J.R.S., B.R.W., K.E.C., G.A.G.), Edinburgh EH16 4TJ, Scotland, United Kingdom"},{"name":"Queens Medical Research Institute, and Edinburgh Preclinical Imaging (M.A.J., A.T., C.M.M.), College of Medicine and Veterinary Medicine, The University of Edinburgh, Edinburgh EH16 4TJ, Scotland, United Kingdom"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jonathan R.","family":"Seckl","sequence":"first","affiliation":[{"name":"British Heart Foundation\/University Centre for Cardiovascular Science (C.I.W., M.A.J., K.M., K.J.M., R.V.R., C.M.M., J.R.S., B.R.W., K.E.C., G.A.G.), Edinburgh EH16 4TJ, Scotland, United Kingdom"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Brian 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