期刊
RENAL FAILURE
卷 38, 期 5, 页码 831-837出版社
TAYLOR & FRANCIS LTD
DOI: 10.3109/0886022X.2016.1160724
关键词
Acute kidney injury; apoptosis; endoplasmic reticulum; ischemic; renal tubular cell
资金
- Natural Science Foundation of China [81170688, 81470973]
- Shandong Province Natural Science Foundation [ZR2014CM040]
Ischemia is the most frequent cause of acute kidney injury (AKI), which is characterized by apoptosis of renal tubular cell. A common result of ischemia in AKI is dysfunction of endoplasmic reticulum (ER), which causes the protein-folding capacity to lag behind the protein-folding load. The abundance of misfolded proteins stressed the ER and results in induction of the unfolded protein response (UPR). While the UPR is an adaptive response, over time it can result in apoptosis when cells are unable to recover quickly. Recent research suggests that ER stress is a major factor in renal tubular cell apoptosis resulting from ischemic AKI. Thus, ER stress may be an important new progression factor in the pathology of ischemic AKI. In this article, we review UPR signaling, describe pathology and pathophysiology mechanisms of ischemic AKI, and highlight the dual function of ER stress on renal tubular cell apoptosis.
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