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These changes were found to be caused by endothelial cell dysfunction rather than a smooth muscle cell defect, as stimulation of mesenteric vessels with the NO donor sodium nitroprusside yielded the same vasodilatory response in CBS +/− and wildtype vessels

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