Journal
JOURNAL OF BONE AND MINERAL RESEARCH
Volume 30, Issue 10, Pages 1831-1839Publisher
WILEY
DOI: 10.1002/jbmr.2527
Keywords
MYOCARDIAL INFARCTION; FGF23; VITAMIN D
Categories
Funding
- Austrian Science Fund [FWF P26534, FWF P24186-B21]
- University of Veterinary Medicine Vienna
- Austrian Science Fund (FWF) [P24186, P26534] Funding Source: Austrian Science Fund (FWF)
- Austrian Science Fund (FWF) [P 24186, P 26534] Funding Source: researchfish
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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-bone-kidney axis that may have important clinical implications and may inaugurate the new field of cardio-osteology. (C) 2015 American Society for Bone and Mineral Research.
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