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Ablation of cardiac TIGAR preserves myocardial energetics and cardiac function in the pressure overload heart failure model.
Am J Physiol Heart Circ Physiol
June 2019
Department of Cardiovascular Medicine, Graduate School of Medical Science, Kyoto Prefectural University of Medicine Kawaramachi-Hirokoji, Kyoto , Japan.
Despite the advances in medical therapy, the morbidity and mortality of heart failure (HF) remain unacceptably high. HF results from reduced metabolism-contraction coupling efficiency, so the modulation of cardiac metabolism may be an effective strategy for therapeutic interventions. Tumor suppressor p53 (TP53) and its downstream target TP53-induced glycolysis and apoptosis regulator (TIGAR) are known to modulate cardiac metabolism and cell fate.
View Article and Find Full Text PDFMethods for the Determination of Rates of Glucose and Fatty Acid Oxidation in the Isolated Working Rat Heart.
J Vis Exp
September 2016
Department of Physiology and Biophysics, Mississippi Center for Obesity Research, Cardiovascular-Renal Research Center, University of Mississippi Medical Center;
The mammalian heart is a major consumer of ATP and requires a constant supply of energy substrates for contraction. Not surprisingly, alterations of myocardial metabolism have been linked to the development of contractile dysfunction and heart failure. Therefore, unraveling the link between metabolism and contraction should shed light on some of the mechanisms governing cardiac adaptation or maladaptation in disease states.
View Article and Find Full Text PDFNew placental factors: Between implantation and inflammatory reaction.
Early Pregnancy (Cherry Hill)
January 2001
The trophoblast invasion is a dynamic changes in cell-cell and cell matrix interaction and it create in the endometrio a reaction similar to the inflammatory reaction. In the recent past most of the investigator in this field had focus on the mediator of this process especially on cytokine and on vasoactive agent. We have studied the inducible isoform of nitric oxide synthase (iNOS), adrenomedullin (AM), fatty acid synthase (FAS), and S-100 protein.
View Article and Find Full Text PDFRate-limiting energy-dependent steps controlling oxidative metabolism-contraction coupling in rabbit aorta.
J Physiol
March 1992
Department of Physiology, University of Pennsylvania School, of Medicine, Philadelphia.
1. We tested the hypotheses that coupling between oxidative metabolism and force in noradrenaline (NOR)-activated rabbit aorta is controlled (a) by an energy-dependent step or steps in receptor-operated coupling mechanisms upstream to myosin light chain (MLC) kinase, or (b) by energy limitation of MLC kinase-mediated phosphorylation of the MLC or actin-activated myosin ATPase. 2.
View Article and Find Full Text PDFPhosphocreatine and oxidative metabolism-contraction coupling in rabbit aorta.
Am J Physiol
August 1989
Department of Physiology, University of Pennsylvania School of Medicine, Philadelphia 19104.
Oxidative metabolism-contraction coupling was studied in single rabbit aortic rings by measuring changes in phosphocreatine (PCr) and ATP content, the ratio of PCr to free creatine (Cr), and changes in muscle force under conditions in which cellular energy production was inhibited. We compared rings with markedly different total PCr content by using rings loaded with creatine, control (unloaded) rings, and rings exposed for 30 min to zero-glucose solution. Creatine loading resulted in increases in PCr content to 300% of control.
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