Researchers find potential mechanisms behind diabetic cardiomyopathy.

Monoamine oxidases, have been shown to play a role in oxidative stress in cells. Monoamine oxidases are enzymes used in mitochondrial membranes and exist as two different variants, MAO-A and MAO-B. Those enzymes have been shown to induce oxidative stress in similar ways, similar to those that result in cardiovascular pathophysiology.

The oxidative damage caused by those enzymes is not fully understood yet. The function of monoamine oxidases involves degradation of monoamines ingested in food and monoamine neurotransmitters like dopamine, serotonin and adrenaline. In the chemical process though, ROS (reactive oxygen species) are produced and contribute to cellular and more specifically mitochondrial dysfunction. There is also focus on the ER (endoplasmic reticulum) and the damage caused to it by ROS, as this has been associated with cardiac pathology. This whole process leads to inflammation that leads to further issues affecting the heart by mediating tissue remodeling among other changes.

Overall, while the mechanisms are known and understood, the connections between them remain unknown. This article hypothesized that MAO is the link that that contributes to all those processes and thus cardiac dysfunction. And indeed the results show that MAO inhibition improves the symptoms of diabetic cardiomyopathy by reducing ROS and it’s associated damage. The researchers found that when MAO was deactivated, oxidative damage and inflammation was limited. This shows that all the cellular processes that lead to diabetic cardiomyopathy are dependent on MAO.

Hyperglycemia can induce stress to mitochondria and the ER, thus induce similar symptoms to that of the MAO. While all those factors contribute to the development of cardiac dysfunction, MAO in this study appears to be the main cause. This study shows how important MAOs are for diabetic cardiomyopathy and that MAO inhibitors could be used not only for heart conditions, but also for diabetics with similar pathologies in clinical trials.

It is interesting to see how such treatments based on MAO inhibition will perform. MAOs degrade neurotransmitters as mentioned above. Overexpression of them not only leads to increased ROS, thus oxidative damage, but also degradation of very important neurotransmitters like serotonin, dopamine and adrenaline. This can have huge effects on psychiatric and neurological disorders. If MAO is overexpressed, like in Brunner syndrome, it can lead to antisocial behaviours, depression and many other psychological disorders. On the other hand, over-inhibition/underexpression of MAO above a certain level may lead to excessive levels of serotonin and then even serotonin syndrome and hypertensive crisis. Mao drugs can act as antidepressants even. Mice without any of the MAO genes display autistic-like traits.

It is clear that MAOs are involved in many cellular pathways and their expression has to be balanced for optimal health. Rather than inhibiting MAOs or overexpressing them, maybe we need to determine which SNPs (single nucleotide polymorphisms), or any other variants affect health. Then, an effective gene therapy may be able to solve issues like diabetic cardiomyopathy. It is relatively early for such drugs but the pathways are logical and the results of such studies do show significant results. It is very interesting to see how future drugs based on MAO inhibition will perform and if they do, how safe that would be.

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Monoamine oxidase-dependent endoplasmic reticulum-mitochondria dysfunction and mast cell degranulation lead to adverse cardiac remodeling in diabetes

Image: By Manu5 –, CC BY-SA 4.0,

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