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Published on: July 21, 2023
Acute cardiac overload does not induce cardiac or skeletal expression of fibroblast growth factor 23 in rats
Abul Fajol1,2, Hirotaka Komaba1,2,3, Chigusa Ishioka1,2
1Division of Nephrology, Endocrinology and Metabolism.
Insights
Acute cardiac overload in rats did not increase fibroblast growth factor 23 (FGF23) levels or expression. This suggests that significant cardiac damage is necessary to induce FGF23 production.
Area of Science:
- Cardiovascular Biology
- Endocrinology
- Mineral Metabolism
Background:
- Elevated fibroblast growth factor 23 (FGF23) is linked to cardiovascular events, including heart failure.
- While FGF23 can induce cardiac hypertrophy, recent findings indicate that cardiac hypertrophy and myocardial infarction stimulate FGF23 production in cardiomyocytes.
Purpose of the Study:
- To investigate if acute cardiac overload increases cardiac and skeletal FGF23 expression.
- To determine if acute cardiac overload elevates circulating FGF23 levels.
Main Methods:
- Acute cardiac overload was induced in rats via intraperitoneal injection of isotonic saline.
- Serum FGF23 levels and mineral metabolism parameters were measured at 2, 6, and 24 hours post-injection.
- Cardiac and skeletal tissue gene expression (FGF23) was analyzed.
Main Results:
- Saline injection successfully induced acute cardiac overload, shown by increased brain natriuretic peptide and atrial natriuretic peptide expression.
- No significant changes were observed in serum FGF23 levels.
- Cardiac, calvarium, and femur FGF23 gene expression remained unchanged.
Conclusions:
- Acute cardiac overload, induced by saline injection in rats, does not elevate FGF23 expression or serum levels.
- These results imply that more severe or prolonged cardiac damage may be required to trigger FGF23 induction.
Abstract:
Elevated fibroblast growth factor 23 (FGF23) is associated with cardiovascular events, particularly heart failure. Although FGF23 has been reported to induce cardiac hypertrophy, recent studies demonstrated that cardiac hypertrophy and myocardial infarction induce FGF23 production by cardiomyocytes. We aimed to explore whether acute cardiac overload increases cardiac and skeletal FGF23 expression and circulating FGF23 levels.
Methods:
We administered 30 μL/g bodyweight of isotonic saline intraperitoneally in rats to induce acute cardiac overload. We measured serum FGF23 levels and other parameters of mineral metabolism at 2, 6, and 24 h after saline or sham injection. We also analyzed gene expression in the heart, calvarium, femur, and kidney at 2 and 24 h after injection.
Results:
Acute saline injection induced cardiac overload as evidenced by a significant upregulation of brain natriuretic peptide along with a trend towards increased expression of atrial natriuretic peptide and mild hyponatremia. However, there were no changes in serum FGF23 levels or FGF23 expression in the heart, calvarium, or femur.
Conclusions:
Acute cardiac overload by saline injection in rats did neither induce FGF23 expression in the heart or bone nor did it increase serum FGF23 levels. These findings suggest that more severe or long-term cardiac damage is required for induction of FGF23 expression.
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