Figure 1.

The role of OS associated with common risk factors and mechanism for ischemic CVD (stroke and CHD) and depression. A–C Obesity, diabetes, and hypertension promote the development of ischemic CVD and depression by increased OS and decreased anti-OS reactions. Moreover, this phenomenon can be reversed by using antioxidants. D OS independently affects stroke via mtDNA, oxLDL, and epithelium and affects CHD via Sirt1/Nrf2 pathway, p38 MAPK pathway, NF-κB/p65 pathway, and PKCα/β2 pathway. E OS facilitates depression by NOX1-derived ROS and prooxidative and proinflammatory events. F Overactive OS contributes to depression, while administrating antioxidants ameliorates depressive symptoms by using gallic acid and green tea in stroke, as well as n-3 PUFA and statins in CHD. G Ischemic patients develop depression through inflammatory reactions. H OS can interact with inflammation through common molecules, such as GSK-3 and NLRP3 inflammasome. I A cascade of reactions in postischemic depression, when OS influences apoptosis through the Bcl-2/Bax pathway and mitochondrial dysfunction in J. K Microbiome-gut-brain axis contributes to the progression of depression in objects with ischemic CVD by impacting the immune system and brain activity as well as by spreading diseases through the enteric nervous system. L Studies have found the role of OS in promoting abnormal protein aggregation, brain lesions, and gut dysbiosis in this axis.