Corrigendum: Renoprotective Effects of Aldose Reductase Inhibitor Epalrestat against High Glucose-Induced Cellular Injury (BioMed Research International (2017) 2017 (5903105) DOI: 10.1155/2017/5903105)

Abstract

Following publication of the article, Renoprotective Effects of Aldose Reductase Inhibitor Epalrestat against High Glucose-Induced Cellular Injury, the authors were made aware that the effects of epalrestat on the high glucosemediated modulation of Akt and ERK pathways were not clear due to the experimental setup. An additional experiment was completed to confirm that the exposure of NRKE cells to mM high glucose (HG)caused a prominent reduction in the phosphorylation of Akt (about %as compared to the control), whichwas prevented in cells coincubated with epalrestat (EPS; ?M) during high glucose exposure. In addition to the original data shown in Figure, this suggests that high glucose conditions acutely activate Akt signalling (within minutes of exposure to high glucose) in renal tubular cells whereas sustained exposure to high glucose decreases Akt activation, which could eventually contribute to tubular cell death. Additionally, the published article incorrectly states that AR inhibition exerts a protective effect on kidney cells through attenuation of Akt and ERK-dependent pathways in Discussion. Please read the corrected statement as follows: Furthermore, the diminished Akt activity in NRK E cells following hours of high glucose exposure (Supplemental Figure) corroborates with the loss of cell viability in these cells (Figure). Interestingly, cotreatment with epalrestat prevented not only the high glucose-induced loss of cell viability but also the diminution of Akt activity in NRKE cells. - 2019 Heba El Gamal et al.