How cardiac cells die — Necrosis, oncosis and apoptosis

Escape mechanisms to protect cardiomyocytes from apoptosis are yet not known for enterovirus infections. Soluble Fas-receptors have to be considered to counteract binding of soluble Fas-ligands that results in the blockade of apoptosis induction. It is a new finding that soluble Fasreceptors were elevated in the presence of enterovirus genome in the heart. Inhibition of apoptosis can impair virus clearing and prolong its replication with a potential worse outcome. In turn, sufficient protection from apoptosis in autoimmune myocarditis should reduce loss of cardiomyocytes. Therefore, the interaction of the Fas components could provide a new therapeutic target in myocarditis.

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SPECT imaging of myocardial infarction using 99mTc-labeled C2A domain of synaptotagmin I in a porcine ischemia–reperfusion model

Fang

Wang

Ji³

et al. 2007

Nuclear Medicine and Biology

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How cardiac cells die — Necrosis, oncosis and apoptosis

Cited by 6 publications

References 8 publications

Molecular Mechanisms of Inherited Ventricular Arrhythmias

Molecular Mechanisms of Inherited Ventricular Arrhythmias

Escape from cardiomyocyte apoptosis by enterovirus persistence due to elevated soluble Fas-receptors

SPECT imaging of myocardial infarction using 99mTc-labeled C2A domain of synaptotagmin I in a porcine ischemia–reperfusion model

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