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Cardiac Adaptation in Heart Failure: Risks due to myocardial by B. Swynghedauw MD, PhD (auth.), Prof. Dr. med. J. Holtz, PD

By B. Swynghedauw MD, PhD (auth.), Prof. Dr. med. J. Holtz, PD Dr. H. Drexler, Prof. Dr. H. Just (eds.)

Traditionally, cardiac hypertrophy is considered an variation of the guts to everlasting mechanical overload. whatever the incontrovertible fact that many various and infrequently unknown fundamental explanations can lead to middle failure, mechanical overload and myocardial hypertrophy is located in just about all varieties of appear continual center failure (apart from failure as a result of extramyocardial obstacles to influx or to relaxation). even though, the reactive expansion of myocardial mass in line with an stronger hemodynamic burden seems to be a double-edged sword. evidently, the hypertrophy is helping to minimize the improved ventricular wall pressure in center failure by way of including contractile devices to the overdistended chamber wall. even if, lately it grew to become transparent that this adaptive hypertrophic procedure is very complicated and will contain difficult points. The adaptive hypertrophy comprises proliferation of the nonmyocyte cardiac cells in addition to big changes within the phenotype of the transforming into myocytes as a result of differential alterations in gene expression.

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J Bioi Chern 266:10023-10026 24. Karliner JS, Kagiya T, Simpson PC (1990) Effects of pertussis toxin on IXI-agonistmediated phosphatidylinositide turnover and myocardial cell hypertrophy in neonatal rat ventricular myocytes. Experientia 46: 81-84 25. King BD, Sack D, Kichuk MR, Hintze TH (1987) Absence of hypertension despite chronic marked elevations in plasma norepinephrine in conscious dogs. Hypertension 9:582-590 Sympathetic modulation of the cardiac myocyte phenotype 29 26. Kohtz D, Dische N, Inagami T, Goldman B (1989) Growth and partial differentiation of presumptive human cardiac myoblasts in culture.

Nominal SREs are observed in other muscle-specific genes including dystrophin, myosin light chain 1/3, cardiac myosin light chain 2, cardiac troponin T, and muscle creatine kinase, where their function relative to other elements is less apparent (please see ref. (41) for complete citations). As nomenclature implies, the fos SRE is a principal target for induction of the fos proto-oncogene by serum factors, which is responsive to multiple agonists including FGFs (59), as well as to proteins implicated in signal transduction such as protein kinase C and c-raf kinase (17).

V) Finally, two proteins that contact SRE 1 - serum response factor (SRF) and a second protein, F-ACT-1, a competitive inhibitor of SRF binding - are readily detected in cardiac myocytes, and are potential common targets for signaling by peptide growth factors, pharmacological agonists, or even mechanical load. Mutational analysis of the F-ACT-1 binding site in SRE1 now enables us to test the hypothesis that F-ACT-1 recognition is a necessary step for the SkA promoter to discriminate between the actions of bFGF and aFGF.

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