As terminally differentiated cells, podocytes exhibit a very limited capacity for self-repair and regeneration. Under pathological conditions, abnormal re-entry of podocytes into the mitotic cycle can induce mitotic catastrophe (MC), resulting in podocyte loss and glomerular structural injury, thereby accelerating the progression of diabetic kidney disease (DKD). This study aimed to elucidate the precise role of NUPR1 in podocyte injury under DKD conditions, investigate its molecular mechanisms in modulating mitotic catastrophe, and assess the potential of NUPR1 as a therapeutic target for treating DKD.
Cai et al. (Wed,) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: