Monoamine Oxidase-Related Vascular Oxidative Stress in Diseases Associated with Inflammatory Burden

Abstract

Monoamine oxidases (MAO) with 2 isoforms, A and B, located at the outer mitochondrial membrane are flavoenzyme membranes with a major role in the metabolism of monoaminergic neurotransmitters and biogenic amines in the central nervous system and peripheral tissues, respectively. In the process of oxidative deamination, aldehydes, hydrogen peroxide, and ammonia are constantly generated as potential deleterious by-products. While being systematically studied for decades as sources of reactive oxygen species in brain diseases, compelling evidence nowadays supports the role of MAO-related oxidative stress in cardiovascular and metabolic pathologies. Indeed, oxidative stress and chronic inflammation are the most common pathomechanisms of the main noncommunicable diseases of our century. MAO inhibition with the new generation of reversible and selective drugs has recently emerged as a pharmacological strategy aimed at mitigating both processes. The aim of this minireview is to summarize available information regarding the contribution of MAO to the vascular oxidative stress and endothelial dysfunction in hypertension, metabolic disorders, and chronic kidney disease, all conditions associated with increased inflammatory burden.

Figure 1

MAO is a mediator of endothelial dysfunction in conditions associated with increased inflammatory burden (hypertension, obesity, diabetes, and chronic kidney disease).

Figure 2

Stimulation with IL-6 (100 ng/ml, 12 h) increases MAO-A expression in mesenteric artery branches harvested from patients undergoing elective abdominal surgery (mRNA level was examined by real-time RT-PCR, n = 6, ^∗p < 0.05 CTL vs. IL6).

Figure 3

Glucose stimulation (400 mg/dl, 12 h) leads to increased MAO-A expression in rat aorta (immunofluorescence: blue—DAPI and red—MAO-A).