Fibroblast growth factor 23—Klotho and hypertension: experimental and clinical mechanisms
| Autor: | Bernardo Rodriguez-Iturbe, Michael Freundlich, Gerardo Gamba |
|---|---|
| Rok vydání: | 2020 |
| Předmět: |
Fibroblast growth factor 23
Nephrology medicine.medical_specialty 030232 urology & nephrology Review 030204 cardiovascular system & hematology urologic and male genital diseases Angiotensin 03 medical and health sciences 0302 clinical medicine FGF23 Internal medicine Renin–angiotensin system Vitamin D and neurology Humans Medicine Tubular sodium handling Renal Insufficiency Chronic Vitamin D Child Klotho Proteins Klotho Glucuronidase Renal sodium reabsorption business.industry Sodium medicine.disease Fibroblast Growth Factors Fibroblast Growth Factor-23 Blood pressure Endocrinology Hypertension Pediatrics Perinatology and Child Health business Kidney disease |
| Zdroj: | Pediatric Nephrology (Berlin, Germany) |
| ISSN: | 1432-198X 0931-041X |
| DOI: | 10.1007/s00467-020-04843-6 |
| Popis: | Hypertension (HTN) and chronic kidney disease (CKD) are increasingly recognized in pediatric patients and represent risk factors for cardiovascular morbidity and mortality later in life. In CKD, enhanced tubular sodium reabsorption is a leading cause of HTN due to augmented extracellular fluid volume expansion. The renin-angiotensin-aldosterone system (RAAS) upregulates various tubular sodium cotransporters that are also targets of the hormone fibroblast growth factor 23 (FGF23) and its co-receptor Klotho. FGF23 inhibits the activation of 1,25-dihydroxyvitamin D that is a potent suppressor of renin biosynthesis. Here we review the complex interactions and disturbances of the FGF23–Klotho axis, vitamin D, and the RAAS relevant to blood pressure regulation and discuss the therapeutic strategies aimed at mitigating their pathophysiologic contributions to HTN. |
| Databáze: | OpenAIRE |
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