Akademik Veri Yönetim Sistemi
Results in Nonlinear Analysis, cilt.8, sa.1, ss.204-225, 2025 (Scopus)
Chronic stress can dysregulate the body’s adaptive stress responses, influencing immune, vascular, and metabolic functions, which are significant in cardiovascular disease risks. This cumulative effect of stress can heighten vulnerability to cardiovascular events, particularly in individuals with existing conditions like diabetes. Repeated stress responses may lead to inflammation, endothelial dys-function, and plaque instability, thereby increasing the risk of atherosclerosis. This article highlights the biochemical stressors with a focus on the mechanistic link towards vascular dysfunction associated with diabetes-mediated stress within a proatherogenic context. Type 2 diabetes causes a spectrum of systemic metabolic dysfunctions with the hallmark features of severe hyperglycemia and associated hyperinsulinemia that both augment oxidative stress and inflammatory responses in the vascular system. These effects are compounded by stress, which induces biochemical stress through the upregulation of reactive oxygen species (ROS). We propose using mathematical modeling to shed light on how stress-induced changes that lead to increased ROS levels and deleterious metabolic pathways further promote plaque formation, contributing to the critical necessity of stress management in attenuating cardiovascular pathologies in diabetic patients. The study highlights the necessity to identify mechanisms of stress-diabetes interactions on atherosclerosis, which may allow new strategies for improving therapeutics.