[Cellular and molecular mechanisms in heart failure].
In patients with heart failure there are distinct functional abnormalities in the myocytes themselves. This review deals with the deteriorations in the myocardial energy metabolism and the recently found alterations in the neurohumoral and hormonal signal transduction and signal realization within the cardiac cells. Beside the reduction in the volume of mitochondria in the overloaded myocardium the energy starvation is also reflected by a decrease in the content of high energy phosphates. Studies on nonfailing and failing human ventricular myocardium identified significant alterations in the neurohumoral regulation of the heart including the fluxes and the transport processes of Ca2+ as well as the beta-adrenoceptors, G-proteins, cAMP levels and cAMP-mediated processes. Recent data on the existence of auto-antibodies against the ADP/ATP translocator of the mitochondrial membrane and of stimulatory acting autoantibodies against i) the L-type calcium channel and ii) the beta 1-adrenoceptor, respectively, in patients with dilated cardiomyopathy, may open a new view in the etiology of heart failure and for consequences in the therapeutic concept of these diseases.
Krause
E G
EG
Institut für Herz-Kreislaufforschung, Berlin-Buch.
D001323:Autoantibodies / Q000502:physiology; D004573:Electrolytes / Q000378:metabolism*; D004734:Energy Metabolism / Q000502:physiology*; D006321:Heart / Q000503:physiopathology; D006333:Heart Failure / Q000503:physiopathology*; D006439:Hemodynamics / Q000502:physiology*; D006801:Humans; D007473:Ion Channels / Q000502:physiology*; D009200:Myocardial Contraction / Q000502:physiology; D015398:Signal Transduction / Q000502:physiology*
D001323:Autoantibodies; D004573:Electrolytes; D007473:Ion Channels
Zelluläre und molekulare Mechanismen bei Herzinsuffizienz.