The failing heart exhibits in-between characteristics of two diverging pathophy-siological conditions: concentric hypertrophy and preserved contractile properties (diastolic dysfunction), and eccentric hypertrophy with enlarged cardiac chambers and impaired: contractile properties (systolic dysfunction). The two hemodynamic variants develop in: response to partially overlapping spectra of cellular signaling cascades, that regulate the expression of a number of genes determining the structure, size, morphology, molecular; regulatory processes of cardiomyocytes, and the properties of the extracellular matrix; altogether the molecular background of myocardial remodelling. From the viewpoint of the: contractile process intracellular Ca2+ homeostasis and contractile proteins deserve specific: attention. Cardiovascular stress mechanisms involve mechanical stimuli and/or binding of well-defined chemical ligands to their respective sarcolemmal receptors, and hence they: mobilize intracellular second messengers to reach the genetic material. Drugs for the intracellular signaling steps to prevent pathologic cardiac remodelling are not yet available.: This is because intracellular pathways leading to heart failure form a network with several parallel downstream paths making pharmacological interventions of this kind hard to succeed.: However, modulation of recently recognized central nodes within this network (e.g. glycogen synthase kinase 3β and histone deacetylases) appears as a promising strategic approach for a more effective heart failure treatment in the future.
|Translated title of the contribution||Pathophysiology and molecular biology of heart failure|
|Number of pages||9|
|Publication status||Published - Dec 1 2010|
ASJC Scopus subject areas