American College of Cardiology Foundation | Journal of the American College of Cardiolo... - 0 views
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Although currently no drugs that specifically target mitochondrial biogenesis in HF are available, acceleration of this process through adenosine monophosphate–activated kinase (AMPK), endothelial nitric oxide synthase (eNOS), and other pathways may represent a promising therapeutic approach
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Mitochondrial biogenesis can be enhanced therapeutically with the use of adenosine monophosphate kinase (AMPK) agonists, stimulants of nitric oxide/cyclic guanosine monophosphate (NO/cGMP) pathway (including phosphodiesteraes type 5 inhibitors), or resveratrol
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Recent evidence suggests that the eNOS/NO/cGMP pathway is an important activator of mitochondrial biogenesis
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BH4 (tetrahydrobiopterin) supplementation can prevent eNOS uncoupling and was found to reduce left ventricular hypertrophy
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folic acid is known to replenish reduced BH4 and has been shown to protect the heart through increased eNOS activity
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Both folate deficiency and inhibition of BH4 synthesis were associated with reduced mitochondrial number and function
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Resveratrol, a polyphenol compound responsible for the cardioprotective properties of red wine, was recently identified as a potent stimulator of mitochondrial biogenesis
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epidemiological studies reveal a reduced risk of cardiovascular disease in premenopausal, but not post-menopausal, women compared with men
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post-menopausal women
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The majority of ROS in the heart appear to come from uncoupling of mitochondrial electron transport chain at the level of complexes I and III
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Because the majority of ROS in HF comes from mitochondria, these organelles are the primary target of oxidative damage.
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cardioprotective therapies such as angiotensin-converting enzyme inhibitors and ATII receptor blockers were shown to possess antioxidant properties, although it is not known whether they target mitochondrial ROS directly or indirectly