By G. Hasenfuss, E. Marbán (auth.), Prof. Dr. med. Gerd Hasenfuss, Eduardo Marbán M.D., Ph.D. (eds.)
G. HASENFUSS, E. MARBAN center failure embodies the important irony of contemporary medication. As we've develop into more and more adept at treating the key proximate explanations of demise in Western society, we've successfully switched over acute sickness into persistent illness. The final 20 years have witnessed a revolution within the therapy of acute coronary syndromes, myocardial infarction specifically. sufferers who succeed in the health facility now have each expectation of leaving alive, yet now not inevitably good. Our skill to blunt the sting of ischemic insults has en gendered new difficulties: a brand new cohort of sufferers whose hearts functionality good sufficient to let non permanent survival, yet on the fee of reduced ex ercise tolerance, dyspnea and elevated long term mortality. The irony is compounded via our more and more subtle pharmacopeia for the deal with ment of middle failure, which, via slowing the development of ventricular dys functionality, has created a prolonged disorder. the actual fact of its chronicity makes center failure no much less lethal. In symptomatic sufferers, mortality exceeds 5-10% in keeping with 12 months regardless of the easiest modern remedy. no longer all middle failure is ischemic, in fact, however the ultimate universal phenotype is eerily concordant whatever the proximate reason. No ask yourself, then, that center failure is the top explanation for hospitalization in the US and in Western Europe and that the superiority of the disorder keeps to upward push. medicines have certainly revolutionized middle failure remedy, ACE inhibitors and beta-adrenergic blockers having the main amazing documents to date.
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Extra info for Molecular Approaches to Heart Failure Therapy
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In mouse aorta, targeted ablation of phospholamban was found to be associated with a marked decrease in sensitivity to both potassium chloride and phenylephrine stimulation. The differences between phospholamban-deficient and wild-type aorta were abolished by SR inhibition [23]. Interestingly, a more recent study demonstrated the existence of phospholam- 45 46 A. G. Schmidt, E. G. Kranias ban in vascular endothelium [40]. Vascular endothelial cells regulate vascular smooth muscle tone through Ca2 + -dependent production and release of vasoactive molecules.
Phospholamban ablation and cardiac function In the first model, the murine phospholamban gene was ablated by homologous recombination technology [27]. The endogenous murine phospholamban-coding region was replaced by the neomycin phosphoribosyl transferase (neo) gene, using gene targeting. Ablation of phospholamban was compatible with life in homozygous mice and at the morphological and histological levels, these mice were indistinguishable from their wild-ty~e littermates. Biochemical studies indicated that the affinity of the SR Ca + ATPase for Ca 2 + was significantly increased in the phospholamban knockout heart compared to wild-type controls.
It is reasonable to assume that such increased activity of GRKs is involved in reduced contractile function, since in transgenic models overexpression of GRK2 [25] or GRK5 [42] results in impaired contractility. P2-Adrenergic receptor overexpression Overexpression of the P2-adrenergic receptor subtype in the heart has been achieved in transgenic mice, where the receptor was expressed under the control of the a-myosin heavy chain (a-MHC) promoter. The line used for most studies shows approximately a 200-fold overexpression of ventricular P2-receptors.
