Introduction Cardiovascular disease is an important factor in the mortality and morbidity of patients with end-stage renal disease receiving hemodialysis. Although mineralocorticoid receptor antagonists may have potential benefits on the cardiovascular system, their safety for patients on hemodialysis remains unclear, considering the differences between the results of already performed clinical trials. Methods MEDLINE, EMBASE, Cochrane, ClinicalTrials.gov and PubMed databases were searched for relevant clinical trials. The Cochrane Collaboration assessment tool was employed to evaluate the quality of the randomized controlled trials. Revman 5.3 was used to perform the meta-analysis. Results Eleven studies (n¼379) were included in the systematic review and five randomized controlled trials were included in the meta-analysis (n¼248). Mineralocorticoid antagonists (MRAs) did not increase predialysis potassium levels significantly (0.11, 95% confidence interval À0.03 to 0.25, p ¼ 0.11). However, the studies included in this review reported inconsistently with respect to effects of mineralocorticoid receptor antagonists on blood pressure, left ventricular ejection fraction and left ventricular hypertrophy, and quantitative analysis was not performed due to insufficient data. One trial showed that the mineralocorticoid receptor antagonists were associated with decreased carotid intima-media thickness and other articles concluded that mineralocorticoid receptor antagonists had no effect on aortic stiffness. Conclusion It is safe to use low dose mineralocorticoid receptor antagonists on patients receiving hemodialysis, at the end of each session of hemodialysis, and close monitoring of serum potassium levels and possible side effects is necessary. The cardiovascular actions still need to be explored and large scale RCTs are in progress.
Objective This study explored the functional interactions between the long non-coding RNA DICER-AS1 and the cellular stress response 1 ( CSR1) gene in gastric cancer. Methods Quantitative polymerase chain reaction (qPCR) and western blotting were used to measure DICER-AS1, CSR1, and miR-650 expression levels. Gastric cancer cell line proliferation and migration abilities were analyzed using the MTT and transwell migration and invasion assays, respectively. Bioinformatic analysis and dual luciferase reporter assays were employed to study the functional interactions among miR-650, DICER-AS1, and CSR1. Results DICER-AS1 and CSR1 expression levels were significantly decreased in gastric cancer tissues compared with normal tissues, and qPCR analysis showed that miR-650 was upregulated in gastric cancer tissues. Bioinformatic analysis and dual luciferase reporter assays revealed that DICER-AS1 functioned as a competing endogenous RNA that sponged miR-650, which in turn regulated CSR1 expression. Importantly, ectopic DICER-AS1 and CSR1 expression inhibited cell proliferation and migration in vitro and suppressed xenograft tumorgenicity in vivo. Conclusions These results suggest that DICER-AS1 functions as a competing endogenous RNA that regulates miR-650 to suppress proliferation and migration of gastric cancer cells by targeting CSR1. These findings indicate that targeting DICER-AS1 and miR-650 could be a novel treatment for gastric cancer.
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