الفهرس 
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Abstract
• The aim of this study is to assess the FGF23/Klotho molecular signaling axis in an experimental model of cardiorenal syndrome type 3 generated by renal artery ligation that causes renal reperfusion ischemia .
• the study was conducted on 12 male Wistar rats, weighing 230– 300g and aged 6–8 months provided from Kasr Al Ainy animal house, Kasr Al Ainy Faculty of Medicine, Egypt.
• The animals were divided into 2 groups, each with six rats: group I (Control) that did not receive any medication and were not subjected to any surgical procedures.
• group II (diseased) where Cardiac Hypertrophy was induced by ligating right renal artery to induce cardiac hypertrophy.
• Serum urea and creatinine, histopathological examination and FGF23, Klotho gene expression in cardiac and renal tissue by quantitative real time PCR were assessed.
• Serum urea levels were within normal ranges while serum creatinine levels were elevated in all diseased rats, they also showed signs of renal ischemia and cardiac hypertrophy in histopathological examination.
• There was a significant Increase regarding the renal FGF23 level in kidney and heart tissues. The higher level was in diseased group. The mean renal FGF23 level was 1.03±0.02 and 6.00±0.62, for Control, diseased, respectively.
• There was a significant difference between the two groups regarding the KOLTHO level in kidney and heart tissues. The lower level was in diseased group. The mean renal klotho level was
1.01±0.01 and 0.25±0.04 for control and diseased groups, respectively.
In Conclusion, there is a significant relation between the molecular signaling pathway FGF23/Klotho and the cardiac and renal disfunctions related to cardiorenal syndrome type three.