Endoplasmic reticulum stress‐induced cell death in podocytes

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Abstract

Endoplasmic reticulum (ER) stress occurs in a variety of pathophysiological mechanisms, and there has been great interest in managing this pathway for the treatment of clinical diseases. Increased ER stress can block integrin-β1 glycosylation, decrease integrin-β1 protein expression and enhance cell death in podocytes. Autophagy is closely interconnected with ER stress to counteract the possible injurious effects related to the impairment of protein folding and is one of the intracellular protein degradation systems. Studies have shown that podocytes exhibit a high rate of autophagy to maintain as terminally differentiated cells. We have attempted to induce autophagy in podocytes with ER stress to increase the longevity of proteins and the degradation of damaged organelles. However, regardless of ER stress or autophagy that protects the cells at early stages, cells cannot adapt to this situation when the stress is already well established, and podocytes will undergo severe injury finally. In summary, ER stress may induce cell death in podocyte, and autophagy mediate to salvage the injuries caused by ER stress in the short term. It seems that adequate, but not excessive, autophagy is crucial to help maintain the cell viability of podocytes.

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