Background and Hypothesis The rehabilitation effect of circuit resistance training in coronary heart disease (CHD) patients remains unclear. We perform this review to examine the rehabilitation effect of circuit resistance training in CHD patients and to provide a basis for the formulation of reasonable individual exercise prescriptions for CHD patients. Methods Randomized controlled trials (RCTs) were searched on PubMed, Web of Science, The Cochrane Library, Embase, Clinical Trials, and CNKI. About 1232 studies were identified. Nine RCTs were finally used for the present meta‐analysis to determine the rehabilitation effect of circuit resistance training in CHD patients, compared to aerobic training. Individuals enrolled for the studies were at a mean age of 60.5 years old and were all CHD patients. Following the PRISMA guidelines, we extracted basic information about the study and patient characteristics, as well as measurements (e.g., the peak oxygen uptake, the body mass index [BMI], the body fat percentage, the systolic blood pressure, the total cholesterol, and triglycerides). Subsequently, this meta‐analysis determined the overall effect by using standardized mean difference (SMD) and 95% confidence interval (CI). Results Compared with aerobic training, circuit resistance training significantly decrease the BMI and the body fat percentage. Conclusions As suggested from the present meta‐analysis of RCTs, circuit resistance training is effective in improving the BMI and the body fat percentage in CHD patients and may help delay the progression of CHD. CRT has the advantage of lower load in most cases with a similar effect.
Objectives Increasing studies have shown that circular RNAs (circRNAs) participate in the pathogenesis and progression of many diseases. However, the function of circRNAs in obstructive sleep apnea (OSA)-induced pancreatic damage has not been fully elucidated. In this study, the altered circRNA profiles in a chronic intermittent hypoxia (CIH) mouse model were investigated, aiming to provide novel clues for delineating the underlying mechanisms of OSA-induced pancreatic injury. Methods A CIH mouse model was established. circRNA microarray was then applied to profile circRNA expression in pancreatic samples from CIH groups and controls. Our preliminary findings were validated by qRT-PCR. Subsequently, GO and KEGG pathway analyses were carried out to annotate the biological functions of target genes of circRNAs. Lastly, we constructed a circRNA-miRNA-mRNA (ceRNA) network according to the predicted circRNA–miRNA and miRNA–mRNA pairs. Results A total of 26 circRNAs were identified to be differentially expressed, with 5 downregulated and 21 upregulated in the CIH model mice. Six selected circRNAs were preliminarily used to confirm the results by qRT-PCR, which were consistent with microarray. GO and pathway analysis indicated that numerous mRNAs were involved in the MAPK signaling pathway. The ceRNA analysis displayed the broad potentials of the dysregulated circRNAs to modulate their target genes by acting as miRNAs sponges. Conclusions Taken together, our study first revealed the specific expression profile of circRNAs in CIH-induced pancreatic injury, which suggested a novel focus for investigating the molecular mechanism of OSA-induced pancreatic damage through modulating circRNAs.
Background: To explore the biological effects of CASC11 on aggravating diabetic nephropathy (DN) by regulating FoxO1 (forkhead transcription factor O1). Methods: Serum levels of CASC11 and FoxO1 in DN patients were detected. The possibility of CASC11 in predicting the onset of DN was analyzed by depicting ROC curves. Correlation between CASC11 and FoxO1 was evaluated by Pearson correlation test. After intervening CASC11 and FoxO1 levels, changes in proliferative and migratory abilities in HG-induced kidney mesangial cells were determinedrespectively. Expression levels of TGF-β1 and Smads regulated by both CASC11 and FoxO1 were examined by Western blot. Results: CASC11 was highly expressed in serum of DN patients, whereas FoxO1 was downregulated, showing a negative correlation. CASC11 may be a diagnostic marker for DN. It attenuated proliferative and migratory abilities in HG-induced kidney mesangial cells, and the inhibitory effects of CASC11 could be abolished by overexpression of FoxO1. Protein levels of TGF-β1 and Smads were positively regulated by CASC11, which were reversed by Smads regulation. Conclusions: Through activating the TGF-β1/Smads signaling, CASC11 inhibits FoxO1 expression and thus induces the aggravation of DN.
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