What is it about?
Here, we explored the effect of OLE in an in vitro model of cardiomyocyte characterized by overexpression of monoamine oxidase-A (MAO-A). This enzyme, by degrading catecholamine and serotonin, produces hydrogen peroxide (H2O2), that causes autophagy dysfunction in cardiomyocytes. We showed that OLE treatment counteracts the toxic effects of the MAO-A/H2O2 axis by autophagy induction involving nuclear translocation of the transcriptional factor EB (TFEB).
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Why is it important?
Our data provide strong evidence of the healthy effect of OLE suggesting its potential use as a nutraceutical agent against age-related pathologies, including cardiovascular diseases, involving autophagy dysfunction.
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This page is a summary of: Oleuropein Aglycone Protects against MAO-A-Induced Autophagy Impairment and Cardiomyocyte Death through Activation of TFEB, Oxidative Medicine and Cellular Longevity, January 2018, Hindawi Publishing Corporation,
DOI: 10.1155/2018/8067592.
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