Advanced glycation end products promote ferroptotic injury in human renal tubular epithelial cells through the miR-362-3p/SLC7A11/GPX4 Axis.
Diabetic nephropathy (DN) is a major cause of chronic kidney disease, yet the mechanisms underlying tubular epithelial injury remain incompletely understood. Advanced glycation end products (AGEs) contribute to diabetic renal damage, but their role in ferroptosis-associated tubular injury is not fully defined. This stu...