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[] However, upon induction of hypertrophy using endothelin-1 and phenylephrine, DNMT3A -knockout (KO) EHTs exhibit compensatory hypertrophy signaling that normalizes contractility, reduces lipid deposits, restores HIF-1 protein levels and glycolytic gene expression, and partially rescues mtDNA and metabolism

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[6] The concentration-response profile of the collagen effect detectable at extremely low concentrations and independent of cell proliferation argues that the intact tripeptide is doing something more specific than passively supplying metal