The regulation of gene expression in myocardial ischemia.
The reaction of the myocytes to ischemic stress is described on the molecular and cell-biological level in this review. It is shown that signalling cascades are activated, that originate most probably simultaneously from cell membrane receptors and from the metabolic derangement in the cytosol. A multitude of signals is transmitted to the nucleus and to the cell membrane which exert different effects with regards to survival and cell death. We describe that death-promoting pathways exist that can be blocked pharmacologically, which leads to an increase in the survival time of ischemic myocardium. In spite of the shortage of energy new mRNA can be produced by ischemic myocardium and hypoxia-specific gene expression also occurs is described. A major difficulty is discussed: mRNA stability can change under hypoxic conditions, which can simulate altered transcription.
Schaper
W
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Department of Experimental Cardiology, Max-Planck-Institute, Bad Nauheim, Germany.
D005786:Gene Expression Regulation; D006360:Heat-Shock Proteins / Q000502:physiology; D006801:Humans; D000860:Hypoxia / Q000235:genetics; D017202:Myocardial Ischemia / Q000235:genetics* / Q000503:physiopathology*; D011401:Promoter Regions, Genetic; D011519:Proto-Oncogenes / Q000502:physiology; D012333:RNA, Messenger / Q000502:physiology; D015398:Signal Transduction / Q000502:physiology*
D006360:Heat-Shock Proteins; D012333:RNA, Messenger