title: Endoplasmic reticulum stress in kidney function and disease.
abstract: OBJECTIVE
  Recently, a number of papers have reported that endoplasmic reticulum (ER) stress is involved in the onset of various kidney diseases, but the pathological mechanisms responsible have not been clarified. In this review, we summarize recent findings on this issue and try to clarify the pathology of ER stress-induced kidney diseases.
  
  
  RESULTS
  ER stress is evoked in various kidney diseases, including diabetic nephropathy, renal fibrosis, inflammation or osmolar contrast-induced renal injury, ischemia-reperfusion, genetic mutations of renal proteins, proteinuria and cyclosporine A treatment. In some cases, chemical chaperones, such as 4-phenylbutyrate and taurodeoxycholic acid, relieve the symptoms, indicating that ER stress-induced apoptosis of renal cells is one of the major causes of certain kidney diseases. Actually, the ER stress response provides protection against some kidney diseases, although the PERK-ATF4-CHOP pathway of the ER stress response is proapoptotic in some kidney diseases. The disposal of unfolded proteins by autophagy is also protective for some ER stress-induced kidney diseases.
  
  
  CONCLUSIONS
  Because ER stress is a major cause of some kidney diseases, the ER stress response and autophagy, which deal with unfolded proteins that accumulate in the ER, are promising therapeutic targets in acute and chronic kidney diseases.
authors.affiliation: Department of Molecular Biochemistry, Graduate School of Life Science, University of Hyogo, Hyogo, Japan.
authors.forename: Mai
authors.initials: M
authors.lastname: Taniguchi
authors.forename: Hiderou
authors.initials: H
authors.lastname: Yoshida
mesh_terms: D000818:Animals; D001343:Autophagy / Q000502:physiology*; D003928:Diabetic Nephropathies / Q000235:genetics / Q000378:metabolism*; D059865:Endoplasmic Reticulum Stress / Q000235:genetics / Q000502:physiology*; D006801:Humans; D007668:Kidney / Q000378:metabolism*; D007674:Kidney Diseases / Q000235:genetics / Q000378:metabolism*; D015398:Signal Transduction / Q000502:physiology