In DKD, ERS is primarily triggered by hyperglycemia, proteinuria, and the presence of AGEs and free fatty acids ( A recent study has revealed that ERS can increase the levels of unsaturated triacylglycerol precursors and reduce lipid droplet formation, leading to tubular injury and fibrosis in renal proximal tubular cell lines and STZ-induced diabetic mouse kidneys (83)
So, how exactly does GHK-Cu get the job done
This redox imbalance promotes the accumulation of lipid ROS and sensitizes cells to ferroptotic death [104, 105]
Angiogenesis & perfusion: Endothelial tube formation and improved blood-flow recovery after ischemia described via VEGFR2-Akt-eNOS signaling (Hsieh 2017)
"The role of homocysteine-lowering B-vitamins in the primary prevention of cardiovascular disease"
GHK-Cu stimulates the formation of new capillaries, which improves tissue perfusion