1999
DOI: 10.1055/s-2007-1013108 View full text |Buy / Rent full text
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Abstract: Transcriptional upregulation of apoptosis-inhibiting genes might be caused by a desensitization to apoptotic stimuli and might indicate a relaxation of the diseased status of the myocardium. These data outline the first biochemical evidence of a remodelling process occurring in supported ventricular myocardium.

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“…13,14 Upregulation of genes associated with cell growth, DNA repair, and apoptosis has been shown in failing hearts after LVAD support. 15 Cytoplasmic levels of cytochrome c, a key mediator of the intrinsic mitochondrial apoptotic pathways, have also been shown to be substantially reduced after LVAD support.…”
Section: Apoptosismentioning
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“…13,14 Upregulation of genes associated with cell growth, DNA repair, and apoptosis has been shown in failing hearts after LVAD support. 15 Cytoplasmic levels of cytochrome c, a key mediator of the intrinsic mitochondrial apoptotic pathways, have also been shown to be substantially reduced after LVAD support.…”
Section: Apoptosismentioning
“…1. Some of these changes include increase in mRNA levels for apoptosis-inhibiting proteins FasEx06del and Bcl-X L [37,38], reduced DNA fragmentation [39,40], upregulation of genes associated with cell growth, DNA repair and apoptosis [41] (an important study showing multiple gene expression changes following LVAD treatment of failing hearts), and reduced cytoplasmic levels of cytochrome c [42]. In contrast, some studies report low levels of apoptosis in failing hearts, with normalization of overexpressed Bcl-2 (an antiapoptotic protein) and PCNA (repair and/or proliferation marker) after LVAD treatment [43].…”
Section: Cell Survival and Apoptosismentioning
“…There are several distinct apoptotic pathways and their regulation is complex. Human HF is generally characterised by loss of cardiomyocytes (Narula et al 2006) but rarely and inconsistently the presence of abundant apoptosis is demonstrated (Francis GS 1999).LVAD support causes normalisation and augmentation of anti-apoptotic proteins FasExo6Del (Bartling et al 1999), BCL-XL levels (Milting et al 1999), BCL-2 (Francis et al 1999), decreased myocardial TNF-α levels (Razeghi et al 2001;Torre-Amione et al 1999), a cytokine believed to possess apoptotic regulatory properties , decreases in markers of DNA fragmentation (Bartling et al 1999), cellular repair (PCNA) (Francis et al 1999) and markers of cellular apoptosis (Baba et al 2000).…”
Section: Cell Survival and Regeneration 231 Apoptosismentioning