Research has shown that GHK Cu: Downregulates TGF-beta1 (the primary pro-fibrotic cytokine) in fibrotic cell models Upregulates decorin a proteoglycan that inhibits TGF-beta1 signalling and organises collagen fibril structure Reduces expression of MMP inhibitors, allowing physiological matrix remodelling to proceed This dual action promoting organised collagen synthesis in healing wounds while suppressing dysregulated fibrotic collagen makes GHK Cu of interest in research models of skin fibrosis, liver fibrosis, and lung fibrosis
After four weeks at 2.5 mg, the dose increases to 5 mg per week
GSH depletion causes ferroptosis in RPE cells To evaluate the mechanism of cell death in GSH-depleted cells, we treated RPE cells with various cell death pathway inhibitors including ferroptosis inhibitors ferrostatin-1 (Fer-1, 8 M), liproxstatin-1 (Lip-1, 600 nM), iron chelator deferoxamine (DFO, 80 M), pan-caspase inhibitor z-VAD-fmk (30 M) to inhibit apoptosis, autophagy inhibitor 3-methyladenine (3-MA, 10 mM), and lysosomal inhibitor bafilomycin A1 (Baf-A1, 75 nM)
JNK:c-Jun N-terminal Kinase