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(1991b)

For example, given the dysregulation of PM GLUT4 processes in insulin resistance described above, future studies could focus on phospho-dysregulated mediators of GLUT4 traffic at the PM such as EFR3A, PI4K, and Cavin proteins (Table 1)

This decline has led some researchers to speculate that reduced GHK signaling could contribute to age-related impairments in: wound healing tissue repair collagen production While this hypothesis remains under investigation, it helps explain why GHK-Cu supplementationparticularly through topical formulationshas become a focus of dermatologic research

Molecules, 27 (16)

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