Why the study?
Does monoamine oxidase inhibition provide cardioprotection against oxidative stress in patients with heart failure and diabetes?
Does monoamine oxidase inhibition provide cardioprotection against oxidative stress in patients with heart failure and diabetes?
This review highlights emerging experimental evidence supporting monoamine oxidase inhibition as a potential cardioprotective strategy to mitigate oxidative stress in heart failure and diabetes.
Oxidative stress is a pathomechanism causally linked to the progression of chronic cardiovascular diseases and diabetes. Mitochondria have emerged as the most relevant source of reactive oxygen species, the major culprit being classically considered the respiratory chain at the inner mitochondrial membrane. In the past decade, several experimental studies unequivocally demonstrated the contribution of monoamine oxidases (MAOs) at the outer mitochondrial membrane to the maladaptative ventricular hypertrophy and endothelial dysfunction. This paper addresses the contribution of mitochondrial dysfunction to the pathogenesis of heart failure and diabetes together with the mounting evidence for an emerging role of MAO inhibition as putative cardioprotective strategy in both conditions.
No takes yet. Share an insight, caveat, or question.
Duicu et al. (2015) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: