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Researchers have reported that MOTS-c treatment prevented the development of heart failure in a mouse model, an effect attributed to AMPK activation in the heart muscle and improvements in mitochondrial function

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Monoamine Oxidase (MAO) Inhibition: Although its clinical relevance is debated, at high doses amphetamine acts as a weak competitive inhibitor of monoamine oxidase, the mitochondrial enzyme responsible for degrading free cytosolic monoamines

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