scholarly journals In vivo Profile of Myocardial Energy Metabolism of Pressure-overloaded Rat.

1993 ◽  
Vol 34 (3) ◽  
pp. 313-331 ◽  
Author(s):  
Satoshi TAKEO ◽  
Kouichi TANONAKA ◽  
Manabu AOKI ◽  
Yasufumi NAKAI ◽  
Atsushi SANBE ◽  
...  
Keyword(s):  
Energy Metabolism ◽  
Myocardial Energy Metabolism

In vivo and in vitro31P MRS studies on myocardial energy metabolism of brain dead cats

2000 ◽  
Vol 11 (1) ◽  
pp. 23-26
Author(s):  
G. J. Brandon Bravo Bruinsma ◽  
J. J. Bredée ◽  
T. J. C. Ruigrok ◽  
C. J. A. Echteld
Keyword(s):  
Energy Metabolism ◽  
Myocardial Energy Metabolism ◽  
Brain Dead

Effects of in Vivo Heart Irradiation on Myocardial Energy Metabolism in Rats

1993 ◽  
Vol 134 (1) ◽  
pp. 79 ◽  
Author(s):  
N. A. P. Franken ◽  
L. Hollaar ◽  
F. J. Bosker ◽  
F. J. M. van Ravels ◽  
A. van der Laarse ◽  
...  
Keyword(s):  
Energy Metabolism ◽  
Myocardial Energy Metabolism

scholarly journals IRF1-mediated downregulation of PGC1α contributes to cardiorenal syndrome type 4

2020 ◽  
Vol 11 (1) ◽  
Author(s):  
Yinghui Huang ◽  
Shaobo Wang ◽  
Jie Zhou ◽  
Yong Liu ◽  
Changhong Du ◽  
...  
Keyword(s):  
Energy Metabolism ◽  
Cardiorenal Syndrome ◽  
Peroxisome Proliferator ◽  
Syndrome Type ◽  
Peroxisome Proliferator Activated Receptor ◽  
Myocardial Energy Metabolism ◽  
Functional Changes ◽  
Myocardial Mitochondria

Abstract Cardiorenal syndrome type 4 (CRS4) is a common complication of chronic kidney disease (CKD), but the pathogenic mechanisms remain elusive. Here we report that morphological and functional changes in myocardial mitochondria are observed in CKD mice, especially decreases in oxidative phosphorylation and fatty acid metabolism. High phosphate (HP), a hallmark of CKD, contributes to myocardial energy metabolism dysfunction by downregulating peroxisome proliferator-activated receptor gamma coactivator 1 alpha (PGC1α). Furthermore, the transcriptional factor interferon regulatory factor 1 (IRF1) is revealed as the key molecule upregulated by HP through histone H3K9 acetylation, and responsible for the HP-mediated transcriptional inhibition of PGC1α by directly binding to its promoter region. Conversely, restoration of PGC1α expression or genetic knockdown of IRF1 significantly attenuates HP-induced alterations in vitro and in vivo. These findings demonstrate that IRF1-PGC1α axis-mediated myocardial energy metabolism remodeling plays a crucial role in the pathogenesis of CRS4.

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