The Role of Oxidative Stress in Common Risk Factors and Mechanisms of Cardio-Cerebrovascular Ischemia and Depression

Abstract

The public health sector faces a huge challenge as a result of the high prevalence and burden of disability caused by ischemic cardio-cerebrovascular disease (CVD) and depression. Although studies have explored the underlying mechanisms and potential therapies to address conditions, there is no treatment breakthrough, especially for depression which is highly influenced by social stressors. However, accumulating evidence reveals that CVD and depression are correlated and share common risk factors, particularly obesity, diabetes, and hypertension. They also share common mechanisms, including oxidative stress (OS), inflammation and immune response, cell death signaling pathway, and microbiome-gut-brain axis. This review summarizes the relationship between ischemic CVD and depression and describes the interactions among common risk factors and mechanisms for these two diseases. In addition, we propose that OS mediates the crosstalk between these diseases. We also reveal the potential of antioxidants to ameliorate OS-related injuries.

Protective Effects of Estrogen on Cardiovascular Disease Mediated by Oxidative Stress

“…Cardiovascular disease (CVD) has the highest mortality in the world [ 1 ]. With the aging of the population and the increasing incidence of obesity and diabetes, the cost of treatment for CVD will significantly increase worldwide [ 2 ]. The incidence of CVD is related to gender, and premenopausal women have a lower incidence of hypertension, atherosclerosis, myocardial dysfunction, ventricular hypertrophy, heart failure, and myocardial ischemia than age-matched men [ 3 ].…”

Pathophysiology and Therapeutic Potential of NADPH Oxidases in Ischemic Stroke‐Induced Oxidative Stress

“…NOX2 activation is mediated by the assembly of four cytoplasmic proteins (p67phox, p40phox, p47phox, and Rac2) with two transmembrane proteins (gp91phox and p22phox), and the activated NOX2 catalyzes oxygen to superoxide through NADPH. 3 Oxidative Medicine and Cellular Longevity WT mice after 72 h of reperfusion, which further indicated that the inhibition or deficiency of NOX2 induced a neuroprotective effect rather than delaying the progression of postischemic brain injury [46]. In a study by De Silva et al, NOX2-deficient mice that underwent 0.5 h of cerebral ischemia and 23.5 h of reperfusion were compared with wild-type mice, and they found that NOX2 deficiency was neuroprotective in the early stage of cerebral ischemia [47].…”

“…Ischemic stroke is by far the most common type of stroke [1] and poses a significant global burden on healthcare. While mortality has improved due to improvements in acute care, poststroke cognitive impairment is an increasing sequela that may eventually develop into dementia [2], and the high prevalence of depression among stroke survivors [3] remains a striking repercussion of stroke, not only with respect to the individual patient but also with respect to the caregivers and healthcare systems as well. Thrombolysis and endovascular therapy are mainstays of contemporary acute stroke treatment [4].…”

Salivary Biomarkers of Oxidative Stress and Inflammation in Stroke Patients: From Basic Research to Clinical Practice

“…Special attention has been paid to redox and inflammatory biomarkers, because oxidative stress and increased cytokine formation play a key role in stroke pathogenesis [ 12 , 13 ]. Indeed, oxygen free radicals are responsible for the oxidation of neuronal lipids, proteins, and nucleic acids, which in turn contributes to oxidative damage of the brain [ 3 , 14 – 16 ].…”