endothelial cell
Moreover, mitochondrial translocation of HO-1 can also lead to localized CO production as a result of heme degradation, thus inhibiting electron flow though mitochondrial electron transport chain complex IV (44). PubMed:26974230
Concentrations of iron, conjugated dienes and lipid hydroperoxides were elevated by about 2- fold in ruptured complicated lesions, as compared to atheromatous lesions (0.433 ± 0.075 vs. 0.185 ± 0.096 nmol Fe/mg tissue; 0.047 ± 0.019 vs. 0.021 ± 0.003 A234 conjugated dienes/mg tissue and 0.465 ± 0.110 vs. 0.248 ± 0.106 nmol LOOH/mg tissue, respectively) and complicated lesions contained 5.6 times more TBARs than atheromatous lesions (0.028 ± 0.012 vs. 0.005 ± 0.001 nmol/mg tissue). PubMed:20378845
This engenders the release of iron, which can promote further the oxidation of plaque lipids through redox cycling reactions. The result of these chemical reactions is the formation of deleterious oxidized ‘gruel’ which, among other things, leads to endothelial oxidative stress and ultimately to cytotoxicity. PubMed:20378845
Thus, by participating in Fenton chemistry, non-transferrin-bound iron (i.e., iron not bound to the physiological iron transport protein, transferrin) causes oxidative damage, cytotoxicity and enhanced endothelial expression of adhesion molecules, thereby enhancing thrombotic risk (Hershko, 2007). PubMed:25307023
Finally, ferrous iron, through Fenton-derived hydroxyl radical species production and protein kinase C function, activates platelets (Iuliano et al, 1994). PubMed:25307023
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If you find BEL Commons useful in your work, please consider citing: Hoyt, C. T., Domingo-Fernández, D., & Hofmann-Apitius, M. (2018). BEL Commons: an environment for exploration and analysis of networks encoded in Biological Expression Language. Database, 2018(3), 1–11.