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In the early stages of DKD, increased hyper-reabsorption and gluconeogenesis expose proximal tubular cells to hypoxia, resulting in mitochondrial dysfunction, increased oxidative stress and tubular injury ( Mitochondria is the primary organelle of in PTECs that is modulated to oxidative stress and hypoxic injury in the diabetic state ( Although there are a large number of in vitro and in vivo studies investigating the mechanism of hypoxia-induced renal tubular damage, due to the lack of non-invasive means, there are few clinical studies that have evaluated renal hypoxia in detail
SLC7A11 is a critical regulatory target involved in VRK2 regulating the GSH metabolic synthesis pathway Aforementioned data indicated that VRK2-deficient PC cells are vulnerable to GSH inhibition, this prompts us to explore the link between VRK2 and GSH metabolic synthesis pathway
European Journal of Cancer
Liposomes are able to pass through the blood-brain barrier to carry their contents directly into neurons
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