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The neuroprotective effect of ACTH(69)PGP was accompanied by a slowdown in the development of delayed calcium dysregulation and synchronous depolarization of mitochondria

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Loss-of-function studies revealed that SELENOT deficiency led to cardiomyocyte death and DNA damage, which were only partially rescued by PSELT, supporting the existence of cross-regulatory mechanisms within the SELENOT/PSELT axis

GHK promotes tissue regeneration and enhances wound healing by activating stemness markers like p63 and PCNA

Both effects operate through pathways that appear independent of the canonical growth hormone receptor