Research Paper Volume 11, Issue 18 pp 7899—7913
Fibroblast growth factor 23 expression in human calcified vascular tissues
- 1 Research Unit, University Hospital Nuestra Señora de Candelaria (UHNSC), Santa Cruz de Tenerife, Spain
- 2 Doctoral and Graduate School, University of La Laguna, San Cristóbal de La Laguna, Tenerife, Spain
- 3 Vascular Surgery Service, UHNSC, Santa Cruz de Tenerife, Spain
- 4 Transplant Coordination, UHNSC, Santa Cruz de Tenerife, Spain
- 5 Pathology Service, UHNSC, Santa Cruz de Tenerife, Spain
- 6 Human Anatomy and Histology Department, University of Salamanca, Salamanca, Spain
- 7 Clinical Analysis Service, UHNSC, Santa Cruz de Tenerife, Spain
- 8 Nephrology Service, UHNSC, Santa Cruz de Tenerife, Spain
- 9 Biomedical Technologies Institute, University of La Laguna, Tenerife, Spain
received: August 9, 2019 ; accepted: September 14, 2019 ; published: September 22, 2019 ;https://doi.org/10.18632/aging.102297
How to Cite
Copyright © 2019 Donate-Correa et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Vascular calcification is a major risk for cardiovascular disease and implies the transformation of smooth muscle cells to an osteoblastic phenotype as a consequence of dysregulation of calcium and phosphate metabolism. Fibroblast growth factor (FGF) 23 is the most potent phosphate regulator. Observational studies suggest that high levels of FGF23 are related to cardiovascular morbidity and mortality. In this work, we determined the levels of both the intact and the carboxi-terminal fragments of circulating FGF23 in 133 patients with established cardiovascular disease, the expression of FGF23, its receptors 1 and 3, and its co-receptor Klotho in vascular fragments of aorta, carotid and femoral in 43 out of this group of patients, and in a control group of 20 organ donors. Patients with atherosclerosis and vascular calcification presented increased levels of FGF23 respect to the control group. Vascular immunoreactivity for FGF23 was also significantly increased in patients with vascular calcification as compared to patients without calcification and to controls. Finally, gene expression of FGF23 and RUNX2 were also higher and directly related in vascular samples with calcification. Conversely, expression of Klotho was reduced in patients with cardiovascular disease when comparing to controls. In conclusion, our findings link the calcification of the vascular tissue with the expression of FGF23 in the vessels and with the elevation of circulating levels this hormone.