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These results suggest that RRTE restores cellular mitochondrial function and attenuates cellular damage caused by lipid disorders by reducing intracellular ROS, reversing MMP, and increasing the mRNA expression of mitochondrial biogenesis markers

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While GHK has been shown to inhibit the inflammatory response and epithelial-mesenchymal transition (EMT) via the TGF-1/Smad 2/3 and IGF-1 pathways in bleomycin-induced fibrosis models [24], its broader anti-inflammatory effects in the context of pulmonary fibrosis pathogenesis may warrant further exploration