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The inflammatory milieu subsequently drives hepatic stellate cell activation and transdifferentiation into myofibroblasts, leading to excessive extracellular matrix deposition and progressive fibrosis, which represents the primary determinant of long-term liver-related outcomes [17]

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In summary, our study primarily investigated the beneficial effects of GHK-Cu in UC, using a DSS-induced colitis mouse model and an in vitro co-culture system, suggesting that GHK-Cu may exert anti-inflammatory properties and its role in facilitating the repair of UC by regulating SIRT1/STAT3 signaling pathway

Annu Rev Pathol 2014