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The association between major depressive disorder (MDD) and cardiovasculardisease (CVD) is among the best described medical comorbidities. The presenceof MDD increases the risk of cardiac admissions and mortality and increases healthcarecosts in patients with CVD, and similarly, CVD affects the course and outcomeof MDD. The potential shared biological mechanisms involved in these comorbidconditions are not well known. However, the enzyme monoamine oxidase-A (MAO-A),which has a key role in the degradation of catecholamines, has been associatedwith the pathophysiology and therapeutics of both MDD and CVD. Increased MAO-Aactivity results in the dysregulation of downstream targets of this enzyme andthus affects the pathophysiology of the two diseases. These deleterious effectsinclude altered noradrenaline turnover, with a direct elevation in oxidative stressparameters, as well as increased platelet activity and cytokine levels. Theseeffects were shown to be reversed by MAO inhibitors. Here, a model describinga key role for the MAO-A in comorbid MDD and CVD is proposed, with focus on theshared pathophysiological mechanisms and the potential therapeutic relevance ofagents targeting this enzyme.

molecular medicine reports

Abnormal function of monoamine oxidase-A in comorbid major depressive disorder and cardiovascular disease: Pathophysiological and therapeutic implications (Review)