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More specifically, the researchers posited that the peptide may have “enhanced the expression of Ki-67 and CD98hc that are less intensively synthesized during cell aging.” Epithalon also seemed to inhibit the activity of Caspase-3, a crucial enzyme believed to facilitate apoptosis (programmed cell death)

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Thus, TMAO-induced inflammation raises the risk of cerebral embolism by causing endothelial damage