The Effect of Endoplasmic Reticulum Stress on Podocyte Apoptosis in Diabetic Nephropathy

Abstract

Diabetic nephropathy (DN) has already become the leading reason for the end-stage renal disease throughout the world. As current therapeutic strategy for progression of DN remained only moderately successful, the underlying mechanisms remain less understood. Endoplasmic reticulum (ER), mitochondria, and death receptor could activate apoptotic pathways, such as caspase-independent pathways. Accumulating evidence indicated that ER stress played a major role in the development and progression of DN. And the aberrant activation of ER stress induced both the inflammation and cellular apoptosis, and modulate the signaling of protective processes including the autophagy. In addition, a growing number of evidences suggested that glomerular podocyte was the key player in DN, and yet the mechanism how ER signaling affected the podocyte apoptosis remained to be well-understood. Because podocytes are terminally differentiated epithelial cells in lack of the capability to proliferate, thus the loss of podocytes is a significant biomarker of progressive kidney diseases, including DN. Hence, the podocyte apoptosis is to be of great significance for the DN treatment. In this review, we summarized relevant apoptotic pathways involved in excessive ER stress-induced apoptosis.

Keywords

• diabetic nephropathy
• endoplasmic reticulum
• podocyte apoptosis