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For example, GLP-1RAs may modulate the CD36-JNK-AP1 pathway by partially down-regulating prolyl 4-hydroxylase subunit alpha-1 (P4HA1), and then inhibit ROS production mediated by Ang II type I receptor, thereby ameliorating cardiac fibroblast proliferation and myocardial fibrosis [167, 168]
doi:10.3109/00365529209000139
The analysis suggests that exposure to GHK-Cu may support inflammatory cell dynamics and neovascular-associated signaling in mammalian models
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