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Myocardial apoptosis in the overloaded and the aging heart: a critical role of mitochondria?
TLDR
Acute stretch of isolated papillary muscle in vitro induces apoptosis, but distension of the extent reported in these in vitro experiments is unlikely.
Apoptosis in the overloaded myocardium: potential stimuli and modifying signals
TLDR
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 gpl30 containing receptors, and from IGF-1.
[Apoptosis--what is it? Significance in coronary heart disease and myocardial infarct].
TLDR
Chronic inhibition of apoptosis for ongoing prevention of myocardial ischemic damage may not become a plausible strategy because of disturbances of the immune system, because of putatively infavorable effects on arteriosclerotic lesions and because of likely disturbances in the physiologic elimination of damaged mitochondria.
757-4 Differential Regulation of Renal Cyclic Nucleotide Phosphodiesterases in Experimental Heart Failure
TLDR
CGMP-POE activity is upregulated in glomeruli in experimental heart failure which may represent a cellular mechanism of ANP resistance in heart failure by inactivating cGMP produced in response to ANP.