By Prof. Dr. L. Thierfelder (auth.), PD Dr. M. Zehender, Prof. Dr. H. Just, Prof. Dr. G. Breithardt (eds.)
From molecule to guy: scientific examine has certainly taken this course, and significant advancements of our realizing of the pathophysiology and epidemiology of affliction were completed. The molecular foundation of the congenital cardiovascular problems has been prolonged from rather few congenital malformations into daily health problems reminiscent of diabetes mellitus, hyperlipoproteinaemea, and arterial high blood pressure. The monogenic and, more challenging, polygenic foundation for an unlimited majority of cardiovascular issues are being outlined extra accurately from yr to yr. This ebook supplies an summary of what has been accomplished to date and defines the present position.
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Additional info for From Molecule to Men: Molecular Basis of Congenital Cardiovascular Disorders
Example text
Distinct phenotype patterns of Ca2+ handling proteins in end-stage failing human hearts Fig. 7. Representative Northern blots showing mRNA expression of SR Ca'+-ATPase (SERCA2a), Na'ICa'+-exchanger (NCXI), atrial natriuretic peptide (ANP), and glyceraldehyde-3-phosphate dehydrogenase (GAPDH) in subepicardium (epi) and subendocardium (endo) in the left ventricular wall from an end-stage failing human heart. i] - n- SERCA2a NCX1 ~-ANP ~-GAPDH Transmural gradients of SR Ca2+·ATPase and Na+/Ca2+·exchanger in failing hearts To test whether variations of gene expression of Ca2+handling proteins in failing hearts may also occur within different regions of the same heart, mRNA levels for SR Ca2+-ATPase and Na+ICa 2+-exchanger were investigated in samples from the epicardial and the endocardial region ofthe left ventricular free wall of 8 end-stage failing hearts.
Furthermore, a very low number of apoptotic myocytes, disseminated in nonischemic myocardial areas of overloaded hearts, is demonstrable in experimental models and in explanted human myocardium. Hemodynamic unloading of terminally failing human hearts by ventricular assist devices reduces the amount of apoptotically cleaved DNA in myocardial extraxts and time-dependently renormalizes the myocardial expression of potentially proapoptotic signal molecules from the apoptotic machinery. While a cellular mechanism for distension-induced myocyte apoptosis in situ is not established, a tentative working hypothesis for the induction of apoptosis in overloaded, nonischemic myocardium postulates the combined actions of impaired mitochondrial function, exaggerated neuroendocrine activity, cytosolic calcium overload, and attenuated survival signals from cytoskeleton, from gp 130 containing receptors, and from IGF-l.
Table 3 lists the death domaincontaining receptors of the TNF receptor family, their cognate ligands, and the competitive antagonists of these receptors. Most ligands of Table 3 exist also as soluble forms, cleaved from their membranes by specific metalloproteases (238), and they can activate their receptors also as soluble ligands, but with less efficacy. Furthermore, death receptor oligomerization with activation of caspases is also possible without interaction with their ligands, for instance under irradiation, which directly oligomerizes death receptors (238).