Endoplasmic reticulum stress‐induced cell death in podocytes

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Endoplasmic reticulum (ER) is responsible for proper folding and processing of the proteins to be secreted, and its capacity to keep the balance of protein folding is vital for the functional integrity of a cell.1 Many situations may disrupt this balance and result in ER stress that is eventually implicated in a variety of clinical diseases, including metabolic diseases,2 neurodegenerative diseases3 and a number of renal pathologies.4 Therefore, ER stress may be a key regulator determining cell survival.9 It is increasingly clear that ER stress leads to the induction of autophagy, a multistep catabolic process to degrade large protein aggregates and damaged organelles in autophagosomes.11 Autophagy is a crucial process that ensures cellular homeostasis and survival through the degradation of cellular proteins and organelles, including mitochondria and ER.12 The seemingly conflicting prosurvival and prodeath roles of autophagy are potentially interchangeable, depending on the interactions between external stimuli and interior cellular ability to maintain survival.13 In this review, we elucidate the role of ER‐stress‐induced podocyte injury and explore the effects of autophagy on podocyte injury.
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