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.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117 J+Geriatr+Cardiol
2015 ; 12
(4
): 439-47
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Significant roles of anti-aging protein klotho and fibroblast growth factor23 in
cardiovascular disease
#MMPMID26347327
Ding HY
; Ma HX
J Geriatr Cardiol
2015[Jul]; 12
(4
): 439-47
PMID26347327
show ga
The klotho gene has been identified as an aging suppressor that encodes a protein
involved in cardiovascular disease (CVD). The inactivation of the klotho gene
causes serious systemic disorders resembling human aging, such as
atherosclerosis, diffuse vascular calcification and shortened life span. Klotho
has been demonstrated to ameliorate vascular endothelial dysfunction and delay
vascular calcification. Furthermore, klotho gene polymorphisms in the human are
associated with various cardiovascular events. Recent experiments show that
klotho may reduce transient receptor potential canonical6 (TRPC6) channels,
resulting in protecting the heart from hypertrophy and systolic dysfunction.
Fibroblast growth factor23 (FGF23) is a bone-derived hormone that plays an
important role in the regulation of phosphate and vitamin D metabolism. FGF23
accelerates urinary phosphate excretion and suppresses 1,25-dihydroxy vitaminD3
(1,25(OH)2D3) synthesis in the presence of FGF receptor1 (FGFR1) and its
co-receptor klotho, principally in the kidney. The hormonal affects of
circulating klotho protein and FGF23 on vascular and heart have contributed to an
understanding of their roles in the pathophysiology of arterial stiffness and
left ventricular hypertrophy. Klotho and FGF23 appear to play a critical role in
the pathogenesis of vascular disease, and may represent a novel potential
therapeutic strategy for clinical intervention.