Abstract Atherosclerosis as one of the crucial causes of cardiovascular diseases (CVD) is the leading reason of death worldwide. One of the contributing factors to this phenomenon is endothelial dysfunction, which is associated with the impact of various agents and their interactions. Tobacco smoke is one of the well known factors here. For better understanding of its significance a model of its impact on atherosclerotic plaque formation has been proposed. The model contains selected aspects of the influence of tobacco smoke, dual function of nitric oxide (NO) (influence of various mechanisms on NO bioavailability), oxidative stress which promotes low density lipoproteins oxidation, macrophages significance and other mechanisms leading to an aggravation of the endothelial disturbances. The model has been built using Petri nets theory and the analysis has been based on t-invariants. This approach allowed to confirm the important role of inflammation and oxidative stress in atherosclerosis development and moreover it has shown the considerable influence of the cigarette smoke.

Abstract The complexity of many biological processes, which, thanks to the development of many fields of science, becomes for us more and more obvious, makes these processes extremely interesting for further analysis. In this paper a quantitative model of the process of macrophage differentiation, which is essential for many phenomena occurring in the human body, is proposed and analyzed. The model is expressed in the language of Petri net theory on the basis of one of the three hypotheses concerning macrophage differentiation existing in the literature. The performed analysis allowed to find an importance of individual factors in the studied phenomenon.