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Altogether these data support the notion that these therapeutic bounties are driven by the agonistic stimulation of myocardial and extra-myocardial CD36 and/or GHSR1a receptors by activating survival pathways, downregulating fibrogenic cytokines, and optimizing energetic homeostasis shunts that cooperate in cellular survival (Hosoda, 2022

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This finding connects to Cognizin's ability to stimulate glutathione in the brain, opening up new oxidative stress-related claims they hadn't previously utilized

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