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Clinical evidence comes in tiers: mechanistic studies (does the molecule do what it should at the cellular level?), animal studies (does it produce the expected effect in a living organism?), and human trials (does it actually work on the people who will use it?)

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The latter binds to RAGE, leading to an increase in NF-B-dependent pro-inflammatory gene expression, suggesting that CML-S100A8/S100A9 generated in inflammatory lesions can elicit a RAGE-dependent inflammatory response (129)

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