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Gewählte Publikation:

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Publikationstyp: Zeitschriftenaufsatz
Dokumenttyp: Originalarbeit

Jahr: 2017

AutorInnen: Slavic, S; Ford, K; Modert, M; Becirovic, A; Handschuh, S; Baierl, A; Katica, N; Zeitz, U; Erben, RG; Andrukhova, O

Titel: Genetic Ablation of Fgf23 or Klotho Does not Modulate Experimental Heart Hypertrophy Induced by Pressure Overload.

Quelle: Sci Rep. 2017; 7(1):11298



Autor/innen der Vetmeduni Vienna:

Andrukhova Olena
Erben Reinhold
Ford Kristopher Robert
Handschuh Stephan
Latic Nejla
Slavic Svetlana
Zeitz Ute

Beteiligte Vetmed-Organisationseinheiten
Institut für Physiologie, Pathophysiologie und Biophysik, Abteilung für Physiologie, Pathophysiologie und experimentelle Endokrinologie
VetCore


Zugehörige(s) Projekt(e): Rolle von FGF23 im akuten Myocardinfarkt


Abstract:
Left ventricular hypertrophy (LVH) ultimately leads to heart failure in conditions of increased cardiac pre- or afterload. The bone-derived phosphaturic and sodium-conserving hormone fibroblast growth factor-23 (FGF23) and its co-receptor Klotho have been implicated in the development of uremic LVH. Using transverse aortic constriction (TAC) in gene-targeted mouse models, we examine the role of Fgf23 and Klotho in cardiac hypertrophy and dysfunction induced by pressure overload. TAC profoundly increases serum intact Fgf23 due to increased cardiac and bony Fgf23 transcription and downregulation of Fgf23 cleavage. Aldosterone receptor blocker spironolactone normalizes serum intact Fgf23 levels after TAC by reducing bony Fgf23 transcription. Notably, genetic Fgf23 or Klotho deficiency does not influence TAC-induced hypertrophic remodelling, LV functional impairment, or LV fibrosis. Despite the profound, aldosterone-mediated increase in circulating intact Fgf23 after TAC, our data do not support an essential role of Fgf23 or Klotho in the pathophysiology of pressure overload-induced cardiac hypertrophy.

Keywords Pubmed: Aldosteronepharmacology
Animals
Biomarkers
Blood Pressure
Cardiomegalydiagnosisetiologymetabolismphysiopathology
Disease Models, Animal
Disease Susceptibility
Fibroblast Growth Factorsbloodgeneticsmetabolism
Fibrosis
Gene Expression Regulation
Gene Knockout Techniques
Glucuronidasegeneticsmetabolism
Mice
Mice, Knockout
Signal Transductiondrug effects
Spironolactonepharmacology

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