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• W3088034110 endingPage "118484" @default.
• W3088034110 startingPage "118484" @default.
• W3088034110 abstract "Chloride channel 7 (CLC-7), broadly expressed in kidney tissues, affects the lysosome degradation pathway. And redox status impairment contributes to cell apoptosis and activates autophagy flux. This study mainly investigates the role and molecular mechanism of CLC-7 in redox status impairment-induced autophagic flux and apoptosis. When NRK52E cells, rat renal tubular epithelial cells, were exposed to H2O2 treatment, apoptosis, autophagy flux, and CLC-7 expression were detected. Further investigation was done to observe the change of apoptosis and autophagy flux in renal cells under overexpression or knocking down of CLC-7. The lysosomes acidity, lysosome enzyme Cathepsin D activity and phosphorylation of Ampk/mTOR were also examined when CLC-7 was overexpressed or knocked down. Redox status impairment induced apoptosis and autophagy flux in NRK52E cells and upregulated CLC-7. Overexpression of CLC-7 increased lysosome acidity and Cathepsin D activity. In cells with CLC-7 overexpression, we observed a significant increase of autophagy flux and decline of apoptosis, as well as an apparent increase of p-Ampk and decrease of p-mTOR. On the contrary, cells with knocking down CLC-7 led to opposite results. CLC-7 is essential to maintain and enhance acidity and enzyme activity in lysosome. Through activating autophagy flux, it exerts survival against renal tubular epithelial cell apoptosis induced by redox status impairment. Its function to modulate Ampk/mTOR pathway is the possible reason why CLC-7 can trigger autophagy flux." @default.
• W3088034110 created "2020-10-01" @default.
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• W3088034110 date "2020-11-01" @default.
• W3088034110 modified "2023-10-06" @default.
• W3088034110 title "Chloride channel 7 protects from redox status impairment-induced renal tubular epithelial cell apoptosis by activating autophagy" @default.
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• W3088034110 doi "https://doi.org/10.1016/j.lfs.2020.118484" @default.
• W3088034110 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/32976885" @default.
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