Destabilization of the human atherosclerotic plaque precedes plaque rupture, which ultimately causes acute myocardial infarction. Ruptured and stable atherosclerotic plaque material was released during primary percutaneous coronary intervention using a distal protection device system. Transcriptome analysis of 2,387 genes of known function identified 89 genes that were differently regulated between ruptured and stable plaque. Overexpression of genes associated with transcription, apoptosis, proliferation, cell-cell interaction and inflammation were observed in ruptured plaque. Transcriptome and immunohistochemical analyses suggest that NFκB activation as well as closely linked up- and downstream events may predispose human atherosclerotic plaques for rupture, which can open new avenues for therapeutic intervention.
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Destabilization of the human atherosclerotic plaque precedes plaque rupture, which ultimately causes acute myocardial infarction. Ruptured and stable atherosclerotic plaque material was released during primary percutaneous coronary intervention using a distal protection device system. Transcriptome analysis of 2,387 genes of known function identified 89 genes that were differently regulated between ruptured and stable plaque. Overexpression of genes associated with transcription, apoptosis, prol...
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