The failing heart is a major source of circulating FGF23 via oncostatin M receptor activation.
Departments of Cardiac Surgery.
Manfred
M
Richter
Anesthesiology, Kerckhoff-Clinic, Benekestrasse, Bad Nauheim, Germany.
Hans-Jürgen
HJ
Lautze
Departments of Cardiac Surgery.
Thomas
T
Walther
Department of Cardiac Development and Remodeling, Max-Planck-Institute for Heart and Lung Research, Bad Nauheim, Germany.
Thomas
T
Braun
Department of Cardiac Development and Remodeling, Max-Planck-Institute for Heart and Lung Research, Bad Nauheim, Germany.
Sawa
S
Kostin
Department of Cardiac Development and Remodeling, Max-Planck-Institute for Heart and Lung Research, Bad Nauheim, Germany.
Thomas
T
Kubin
D000818:Animals; D002478:Cells, Cultured; D000089703:Fibroblast Growth Factor-23; D005346:Fibroblast Growth Factors / Q000097:blood / Q000378:metabolism*; D006333:Heart Failure / Q000503:physiopathology*; D006801:Humans; D051379:Mice; D053677:Receptors, Oncostatin M / Q000502:physiology*
C000717427:FGF23 protein, human; C000717428:Fgf23 protein, mouse; D053677:Receptors, Oncostatin M; D005346:Fibroblast Growth Factors; D000089703:Fibroblast Growth Factor-23