FGF23 and its effects on the heart
Fibroblast growth factor 23 (FGF23) is a hormone primarily known for its role in mineral metabolism, particularly in regulating phosphate homeostasis.
FGF23 is primarily produced in the bone by osteocytes and acts on the kidneys to regulate phosphate reabsorption and vitamin D metabolism. FGF23 helps to maintain phosphate levels within the normal range by promoting urinary phosphate excretion and inhibiting the production of vitamin D (1). The dysregulation of FGF23 can lead to conditions such as hypophosphatemic rickets and hyperphosphatemia.
FGF23 and its effects on the heart
Numerous clinical studies have shown that elevated plasma level concentrations of FGF23 are linked to left ventricular hypertrophy (LVH), heart failure, and increased mortality in the general population, particularly among individuals with chronic kidney disease (CKD) (2). The exact mechanisms by which FGF23 affects the heart are still under investigation, but several possible pathways have been suggested. For instance, FGF23 may induce hypertrophy directly through binding to specific FGF23 receptors expressed by cardiomyocytes in the heart. FGF23 may also promote hypertrophy indirectly by altering mineral metabolism, leading to increased circulating levels of phosphorus, which can contribute to cardiovascular damage.
In addition, FGF23 may have effects on the endothelium, the inner lining of blood vessels. It has been suggested that FGF23 may hinder endothelial function and promote vascular calcification, thereby contributing to the development of cardiovascular disease. Further research is needed to fully understand the exact mechanisms through which FGF23 affects the heart and its role in cardiovascular disease (3).
Measurement of FGF23
FGF23 concentrations can be measured with blood tests. The most common way for measuring FGF23 is with a conventional ELISA assay (enzyme-linked immunosorbent assay). The ELISA utilizes specific antibodies that recognize and bind FGF23 molecules present in the sample. The intensity of the antibody-antigen reaction is measured, allowing an easy quantification of FGF23 in the respective sample.
Currently there are two different assays that allow the measurement of FGF23 in blood samples:
Intact FGF23 Assays
intact FGF23 represents the full length, biologically active form of the hormone. It consists of the complete FGF23 protein structure without being enzymatically cleaved.
The BIOMEDICA FGF23 (intact) human ELISA (cat. no. BI-20700)
is a sandwich-based immunoassay with an anti-human FGF23 capture antibody recognizing a structural epitope in the N-terminal part of FGF23 and a detection antibody binding to the C-terminal part of mature FGF23.
FGF23 C-terminal Assays
The c-terminal fragments of FGF23 are the result of the enzymatic cleavage of the intact FGF23 molecule.
Of note: all commercially available FGF23 c-terminal assays detect both c-terminal FGF23 fragments as well as the intact FGF23 molecule!
The BIOMEDICA FGF23 (C-terminal) human multi-matrix ELISA (cat. no. BI-20702)
is a sandwich-based immunoassayw hich recognizes multiple epitopes in the C-terminal part of FGF23.
Features & Benefits
- Validated ELISA kits following international quality guidelines
- Biomedica´s FGF23 assay have been used in numerous studies
validation reports and citations can be downloaded here
Literature
- Biology of Fibroblast Growth Factor 23: From Physiology to Pathology. Courbebaisse M, Lanske B. Cold Spring Harb Perspect Med. 2018 May 1;8(5):a031260. doi: 10.1101/cshperspect.a031260. PMID: 28778965; PMCID: PMC5932574.
- Direct and indirect effects of fibroblast growth factor 23 on the heart. Nakano T, Kishimoto H, Tokumoto M Front Endocrinol (Lausanne). 2023 Feb 24;14:1059179. doi: 10.3389/fendo.2023.1059179. PMID: 36909314; PMCID: PMC9999118.
- FGF23 directly impairs endothelium-dependent vasorelaxation by increasing superoxide levels and reducing nitric oxide bioavailability. Silswal N, Touchberry CD, Daniel DR, McCarthy DL, Zhang S, Andresen J, Stubbs JR, Wacker MJ. Am J Physiol Endocrinol Metab. 2014 Sep 1;307(5):E426-36. doi: 10.1152/ajpendo.00264.2014. Epub 2014 Jul 22. PMID: 25053401; PMCID: PMC4154070.