Key result
Experimental evidence suggests that targeting peptides involved in endothelial dysfunction and reperfusion injury with antagonists or antibodies may protect against myocardial cell damage.
Targeting specific peptides involved in endothelial dysfunction during ischemia-reperfusion may offer new therapeutic strategies for coronary heart disease.
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May identify peptide targets for reperfusion injury; leaves open clinical translation in coronary disease.
Promising approaches towards new therapeutic strategies in coronary heart disease might emerge from an improved pathophysiological understanding of the role of certain peptides, which require a localizing event for their accumulation or expression in the coronary vasculature. Temporal myocardial ischaemia or hypoperfusion with reperfusion are such localizing acute events, which induce endothelial dysfunction and subsequent tissue damage in the affected myocardium. Peptides involved in these pathological processes are elements of the complement system, cell adhesion molecules on endothelial cells and on leukocytes, endothelial proteins affecting the coagulation cascade, and enzymes contributing to endothelial production of cytokines or superoxide anion. Protection against postischaemic reperfusion damage of the endothelium by antagonists or antibodies can be shown in experiments, and this endothelial protection appears crucial for reducing myocardial cell damage.
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Holtz et al. (1991) conducted a review in Coronary heart disease. Peptide antagonists or antibodies was evaluated. Experimental evidence suggests that targeting peptides involved in endothelial dysfunction and reperfusion injury with antagonists or antibodies may protect against myocardial cell damage.
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