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Aldosterone exerts an enormous function on proximal tubular cells (PTC) senescence, which is a common pathomechanism contributing to renal dysfunction. Numerous studies have shown that oxidative stress is deeply involved in the pathophysiologic processes of chronic kidney diseases. The study aims to investigate whether autophagy could regulate the process of senescence through oxidative stress in PTC both in vivo and ex vivo. Our results suggested that aldosterone treatment increased the senescence and oxidative stress as evidenced by increased percent of SA-β-Gal positive cells, reactive oxygen species level, expression of NADPH oxidase 4 (NOX4) rather than NOX2, and the up-regulation of p21 in cultured PTC. Furthermore, the alternation of the expression of p62 and LC3-II/LC3-I demonstrated that aldosterone treatment remarkably influenced autophagic flux. NOX4 siRNA treatment or autophagy induction with rapamycin reduced the oxidative stress and senescence in aldosterone-induced PTC. On the contrary, inhibition of autophagy with chloroquine worsened these changes. Similar results were further confirmed in vivo. Our results suggested that autophagy may become a realistic therapeutic strategy against aldosterone-induced PTC injury via improving oxidative stress.

Objective The present study investigated whether hemodialysis (HD) patients exhibit future memory impairment (PM; the capability of remembering to perform expected future actions) and exploring relevant factors of PM task performance. Methods Sixty HD patients and 60 healthy controls matched by age are enrolled in the Mini-Mental State Examination (MMSE), Finger Span Test (DST), Oral Fluency Test (VFT), Ray Auditory Oral Learning Test (RAVLT), Received Stroop Color Word Interference Test (SCWT), and event-based PM (EBPM) and time-based PM (TBPM). Results There were no significant difference between the patients and controls in the DST-Forward digit span (9.00 ± 1.25 versus 8.97 ± 1.33, p = 0.96), the DST-Backward digit span (5.23 ± 1.98 versus. 4.60 ± 1.65, p = 0.11), the RAVLT of delayed recall (7.28 ± 2.36 versus 6.87 ± 3.33, p = 0.09) and the VFT for animals (16.70 ± 3.50 versus 17.68 ± 5.45, p = 0.56). By comparison, patients had a much worse performance than controls on the MMSE (29.10 ± 0.84 versus 28.33 ± 0.77, p