The iron overload caused by non-enzymatically glycated transferrin triggers oxidative stress and ferroptosis by regulating the PI3/AKT signaling pathway and the expression of Nrf2 to promote renal damage in diabetes.
Non-enzymatic glycation is an important post-translational modification of proteins, ultimately forming advanced glycation end products (AGEs). In a high-glucose environment, the glycation degree of transferrin (Tf) increases, leading to elevated levels of AGE-modified transferrin (AGE-Tf), which reduces the binding ca...