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Effects in active malignancy are not well characterized, and most clinicians treat this as an exclusion until more data exists
Conversely, TMAO can release inflammatory factors (caspase-1, IL-1 ) (49) in a dose-and time-dependent manner by activating the reactive oxygen species (ROS)thioredoxin-interacting protein (TXNIP) NLRP3 signaling pathway (50) and inhibiting sirtun3 (SIRT3) superoxide dismutase2 (SOD2)mitochondrial ROS signaling pathway (51), thereby causing endothelial cell injury and aggravating the formation and development of atherosclerosis
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Long-term safety in injectable use is not well characterized in published trials
Clinical and laboratory reviews and studies show improvement in total/progressive motility and reduced DNA damage after Myo-inositol administration
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