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In the LPS-induced acute lung injury mouse model, treatment of GHK-Cu also significantly suppressed TNF- and IL-6 expression with a significant decrease of both NF-B p65 and p38 MAPK signaling, suggesting that GHK-Cu is useful for the development of novel anti-inflammatory therapies [22]

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In uremia, a defect in the post-receptor GH-activated JAK2 signal transducer and STAT transduction is described as one of the mechanisms of GH resistance [14]

GHK-Cu elicits in vitro, dose-dependent transcriptional alterations in pathways relevant to extracellular matrix composition

doi: 10.1016/j.rbmo.2010.03.008 119 LafuenteRGonzlez-ComadrnMSolILpezGBrassescoMCarrerasRet al