Psychiatric disorders (i.e., depression and schizophrenia) show high rates of comorbidity with cardiovascular (i.e., coronary heart disease) and cerebrovascular (i.e., stroke) disturbances. The bond between these disorders is apparent in clinical practice. In fact, depression and anxiety independently predict cardiac events, which in turn represent a major cause of mortality in psychiatric disorders, the latter being frequently burdened by cerebrocardiovascular risk factors (i.e., smoking). On the other hand, depressive symptoms are extremely common in poststroke and vascular dementia. Interestingly, the link between cerebrocardiovascular and psychiatric disturbances could find an explanation at a molecular level, since both disorders share oxidative stress (OS) as a major contributor to their pathogenesis and progression.

From a cardiovascular perspective, OS is involved in the pathogenesis of several risk factors (i.e., obesity and hypertension), alters the function of blood vessels (damaging the vascular endothelium), and contributes to cardiac remodelling following myocardial infarction. Hence, a prooxidative condition favours the occurrence of cardiovascular disease but also its progression, being involved in the maladaptive response to cardiac injury.

Looking at neuropsychiatric aspects, OS contributes to the neuronal apoptosis and the disruption of the blood-brain barrier characterizing stroke, vascular dementia, and subarachnoid haemorrhage. On the other hand, it is involved in the pathogenesis of several psychiatric disorders (i.e., depression, bipolar disorder, and schizophrenia) through various mechanisms, such as synaptic alteration and circadian rhythm disruption.

Finally, from a molecular point of view, depressed patients frequently display a prooxidative profile favouring atherosclerosis (i.e., enhanced NADPH oxidase activity and high endoplasmic reticulum stress). In addition, hyperhomocysteinemia, a cerebrocardiovascular risk factor triggering OS, has been reported among patients suffering from schizophrenia. As a matter of fact, both psychiatric and cerebrocardiovascular disorders share OS as a common molecular basis, as well as several OS-related molecular abnormalities, such as enhanced oxidation of lipoproteins, low paraoxonase activity, and dysfunctional glycogen synthase kinase-3 beta. Interestingly, the proinflammatory and prooxidative properties of certain drugs could even explain why some psychopharmacological agents (such as antipsychotics) display a potential cardiotoxicity (i.e., QTc prolongation), while cardiac medications, such as reserpine and class I antiarrhythmics, could, respectively, lead to depressive and psychotic symptoms.

In this special issue, we are inviting researchers to contribute research articles and review articles that seek to address the role of oxidative stress as a link between cerebrocardiovascular and psychiatric disorders.

Potential topics include but are not limited to the following:

• Occurrence and response to cardiac injury: the role of oxidative stress
• Functional alterations of blood vessels: the role of oxidative stress
• Oxidative stress and vascular dementia
• Oxidative stress and poststroke depression
• Oxidative stress and psychiatric drugs-induced cardiologic side effects
• Oxidative stress and cardiologic drugs-induced psychiatric side effects
• Oxidative stress as a link between cerebrocardiovascular and psychiatric disturbances