{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,2,13]],"date-time":"2026-02-13T07:39:31Z","timestamp":1770968371432,"version":"3.50.1"},"reference-count":45,"publisher":"Oxford University Press (OUP)","issue":"10","license":[{"start":{"date-parts":[[2024,2,3]],"date-time":"2024-02-03T00:00:00Z","timestamp":1706918400000},"content-version":"vor","delay-in-days":3222,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2015,10,1]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n               <jats:sec>\n                  <jats:title>\u2003<\/jats:title>\n                  <jats:p>Myocardial infarction (MI) is a major cause of death worldwide. Epidemiological studies have linked vitamin D deficiency to MI incidence. Because fibroblast growth factor-23 (FGF23) is a master regulator of vitamin D hormone production and has been shown to be associated with cardiac hypertrophy per se, we explored the hypothesis that FGF23 may be a previously unrecognized pathophysiological factor causally linked to progression of cardiac dysfunction post-MI. Here, we show that circulating intact Fgf23 was profoundly elevated, whereas serum vitamin D hormone levels were suppressed, after induction of experimental MI in rat and mouse models, independent of changes in serum soluble Klotho or serum parathyroid hormone. Both skeletal and cardiac expression of Fgf23 was increased after MI. Although the molecular link between the cardiac lesion and circulating Fgf23 concentrations remains to be identified, our study has uncovered a novel heart\u2013bone\u2013kidney axis that may have important clinical implications and may inaugurate the new field of cardio-osteology. \u00a9 2015 The Authors. Journal of Bone and Mineral Research published by Wiley Periodicals, Inc. on behalf of American Society for Bone and Mineral Research (ASBMR).<\/jats:p>\n               <\/jats:sec>","DOI":"10.1002\/jbmr.2527","type":"journal-article","created":{"date-parts":[[2015,4,9]],"date-time":"2015-04-09T22:49:02Z","timestamp":1428619742000},"page":"1831-1839","source":"Crossref","is-referenced-by-count":83,"title":["Experimental Myocardial Infarction Upregulates Circulating Fibroblast Growth Factor-23"],"prefix":"10.1093","volume":"30","author":[{"given":"Olena","family":"Andrukhova","sequence":"first","affiliation":[{"name":"University of Veterinary Medicine ViennaViennaAustria"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Svetlana","family":"Slavic","sequence":"additional","affiliation":[{"name":"University of Veterinary Medicine ViennaViennaAustria"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Kathrin I","family":"Od\u00f6rfer","sequence":"additional","affiliation":[{"name":"University of Veterinary Medicine ViennaViennaAustria"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Reinhold G","family":"Erben","sequence":"additional","affiliation":[{"name":"University of Veterinary Medicine ViennaViennaAustria"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"286","published-online":{"date-parts":[[2015,4,9]]},"reference":[{"key":"2024020319021351500_jbmr2527-bib-0001","doi-asserted-by":"crossref","first-page":"1636","DOI":"10.1016\/j.amjcard.2011.01.048","article-title":"Prevalence of vitamin D deficiency in patients with acute myocardial infarction","volume":"107","author":"Lee","year":"2011","journal-title":"Am J Cardiol"},{"key":"2024020319021351500_jbmr2527-bib-0002","doi-asserted-by":"crossref","first-page":"713","DOI":"10.1016\/j.amjhyper.2007.01.017","article-title":"Serum 25-hydroxyvitamin D, ethnicity, and blood pressure in the Third National 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