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Vitamin D-Parathyroid Hormone-Fibroblast Growth Factor 23 Axis and Cardiac Remodeling
1Special Demand Medical Care Ward, Beijing Anzhen Hospital Jilin Hospital (Changchun Central Hospital), Changchun, China.
Insights
Vitamin D deficiency, hyperparathyroidism, and high FGF23 levels create a cycle that worsens cardiac remodeling in heart failure. Understanding this axis is key to improving heart function and treating patients.
Area of Science:
- Cardiology
- Endocrinology
- Metabolic Diseases
Background:
- Cardiac remodeling is a response to heart failure (HF) that alters heart structure and function.
- Nutritional and metabolic diseases can worsen cardiac remodeling.
- Vitamin D deficiency, hyperparathyroidism, and FGF23 are implicated in cardiac remodeling progression.
Purpose of the Study:
- To explain the effects of vitamin D deficiency, hyperparathyroidism, and FGF23 on cardiac remodeling.
- To highlight the significance of the vitamin D-parathyroid hormone-FGF23 axis in managing heart remodeling.
- To contribute to improved treatment strategies for heart failure patients.
Main Methods:
- Review of existing literature on the roles of vitamin D, parathyroid hormone, and FGF23 in cardiac remodeling.
- Analysis of the pathophysiological mechanisms linking these factors to heart disease.
- Synthesis of evidence regarding the vicious cycle between these factors.
Main Results:
- Vitamin D deficiency activates RAAS, promoting inflammation and fibrosis.
- Hyperparathyroidism exacerbates cardiac remodeling through various pathways, including RAAS activation and oxidative stress.
- FGF23 directly contributes to ventricular hypertrophy and myocardial fibrosis, forming a detrimental cycle with vitamin D deficiency and hyperparathyroidism.
Conclusions:
- The interplay between vitamin D deficiency, hyperparathyroidism, and elevated FGF23 creates a vicious cycle driving cardiac remodeling.
- Targeting this axis offers a potential therapeutic strategy for improving or reversing cardiac remodeling in heart failure.
- Understanding this endocrine-cardiac axis is crucial for advancing HF treatment.
Abstract:
Cardiac remodeling is a compensatory adaptive response to chronic heart failure (HF) altering the structure, function, and metabolism of the heart. Many nutritional and metabolic diseases can aggravate the pathophysiological development of cardiac remodeling. Vitamin D deficiency leads to cardiac remodeling by activating the renin-angiotensin-aldosterone system (RAAS), resulting in enhanced inflammation and directly promoting cardiac fibrosis and extracellular matrix deposition. Hyperparathyroidism upregulates protein kinase A or protein kinase C, enhances intracellular calcium influx, promotes oxidative stress, activates RAAS, and increases aldosterone levels, thereby aggravating cardiac remodeling. Besides, fibroblast growth factor 23 (FGF23) plays a direct role in the heart, resulting in ventricular hypertrophy and myocardial fibrosis. Vitamin D deficiency leads to hyperparathyroidism, which in turn increases the level of FGF23. Elevated levels of FGF23 further inhibit vitamin D synthesis. Evidence exists that vitamin D deficiency, hyperparathyroidism, and marked elevations in FGF23 concentration form a vicious cycle and are believed to contribute directly to cardiac remodeling. Therefore, the purpose of this article is to introduce the specific effects of the above substances on the heart and to explain the significance of understanding the vitamin D-parathyroid hormone-FGF23 axis in improving or even reversing cardiac remodeling, thus contributing to the treatment of patients with HF.
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