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There's no strong theoretical reason to weight angiogenesis more heavily than cell migration (or vice versa) in tissue-repair research both are prerequisites for repair, both contribute distinct mechanisms, and neither obviously dominates the other in published research models
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The central theory behind AOD-9604s action revolves around its ability to enhance the breakdown of fats (lipolysis) while reducing the formation of new fat (lipogenesis)
In adipocytes, NNMT inhibition elevates NAD and SAM and suppresses de novo lipogenesis in a concentration-dependent manner, consistent with on-target activity [13]
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