Poster: "Selected aspects of the participation of tobacco smoke in the development of atherosclerosis modeled and analyzed using Petri nets."
Abstract: Endothelial dysfunction is induced by a various factors, some of them are: high blood pressure, high glucose level (in diabetes), high low-density lipoprotein level (LDL) and smoking in the wider sense of the term. For a better understanding of
the influence of cigarette smoking on endothelial damage, stimulating inflammation and prothrombotic states a model of this complex biological process has been presented. The
proposed model has been built using Petri nets . This Petri net structure includes indirect effect of cigarette smoke on impairment of endothelial function, caused by among
others changing the lipid profile (it leads to increase the amount of LDL and then to the LDL oxidation, which in result promotes atherosclerosis), decrease the amount of tetrahydrobiopterin (BH4) (it has influence on inhibition of nitric oxide (NO) synthesis, because BH4 is a cofactor for endothelial nitric oxide synthase, which is necessary for
NO synthesis), increase the amount of many other important factors, which influence on the development of unwanted processes (oxidative stress, oxidation of LDL, proliferation
of vascular smooth muscle cells) . In addition, smoking stimulates inflammation and prothrombotic states, which lead to the development of atherosclerosis. For this reason,
the model includes the harmful effects of macrophages (which stimulates development of plaque) and dual role of NO (which is dependent on the amount of this molecule). The
analysis of the proposed model has been based mainly on t-invariants. To determine the biological sense of the model, analysis of cluster of t-invariants has been performed
This research has been partially supported by the Polish National Science Centre grant
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