
Aggregation
Autophagy
Ca(2+)
Cancer
Cellular stress
c-Fos
Chaperones
c-myc
Degradation
E3 ligases
Heat shock
Hsp40
Hsp70
Hsp90
Hypoxia
IFN
IGF
Inflammation
LC3
mTor
Neurodegeneration
NFkappaB
Oxidative stress
Parkinson's
Proteases
Proteasome
Protein folding
Protein misfolding
ROS
Tau
Ubiquitin
UPR

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Endoplasmic reticulum stress as a progression factor for kidney injury
Curr. Opin. Pharmacol. 2010, view full abstract in PubMed
Dysfunction of endoplasmic reticulum (ER) maintaining protein homeostasis can result from various disturbances, including hypoxia or oxidative stress, which lead to an imbalance between protein-folding capacity and protein-folding load. This in turn leads to ER stress and induction of the unfolded protein response (UPR). The UPR initially serves as an adaptive response, but also induces apoptosis in cells under severe or prolonged ER stress. Accumulating evidence indicates that ER stress contributes to glomerular and tubular damages in kidney disease. These findings emphasize the importance of ER stress as a new progression factor and the interesting future possibility of renoprotective strategies targeting ER stress. These therapeutic approaches may act by breaking the vicious cycle of oxidative stress, hypoxia, and ER stress.