Fibroblast Growth Factor 23

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How fibroblast growth factor 23 works.

There is a discontinuum of hereditary and acquired disorders of phosphate homeostasis that are caused by either high or low circulating levels of the novel phosphaturic hormone fibroblastic growth factor 23 (FGF23). Disorders that are caused by high circulating levels of FGF23 are characterized by hypophosphatemia, decreased production of 1,25-dihydroxyvitamin D, and rickets/osteomalacia. On th...

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MicroRNA-297a regulates vascular calcification by targeting fibroblast growth factor 23

Objective(s): Vascular calcification is one the major characteristics in patients with various types of chronic inflammatory disorders. MiRNAs have been shown to be involved in many normal biological functions as well as diseases; however, their role in vascular calcification has not received much attention. Materials and Methods: In the current study, we built a vascular calcification rat mode...

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Update on Fibroblast Growth Factor 23 in Chronic Kidney Disease

Chronic kidney disease (CKD) is a public health epidemic that affects millions of people worldwide. Presence of CKD predisposes individuals to high risks of end-stage renal disease (ESRD), cardiovascular disease, and premature death. Disordered phosphate homeostasis with elevated circulating levels of fibroblast growth factor 23 (FGF23) is an early and pervasive complication of CKD. CKD is like...

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Fibroblast Growth Factor–23 and Cardiac Structure and Function

BACKGROUND Fibroblast growth factor-23 (FGF-23) is a phosphaturic factor previously associated with left ventricular hypertrophy and systolic dysfunction among individuals with chronic kidney disease. Whether FGF-23 acts directly to induce left ventricular hypertrophy, potentially independent of its klotho coreceptor, remains uncertain. We investigated associations of FGF-23 with cardiac struct...

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The Role of Fibroblast Growth Factor-23 in Cardiorenal Syndrome

Abnormalities in chronic kidney disease-related bone and mineral metabolism (CKD-MBD) have emerged as novel risk factors in excess cardiovascular mortality in patients with CKD and end-stage renal disease (ESRD). The pathophysiological links between CKD-MBD and adverse cardiovascular events in this patient population are unclear. Hyperphosphatemia through induction of vascular calcifications an...

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ژورنال

عنوان ژورنال: Circulation

سال: 2014

ISSN: 0009-7322,1524-4539

DOI: 10.1161/circulationaha.114.011034