A network meta-analysis comparative the efficacy of angiotensin-converting enzyme inhibitors and calcium channel blockers in hypertension.

BACKGROUND: Currently, most studies primarily focus on directly comparing the efficacy and safety of angiotensin-converting enzyme inhibitors (ACEIs) and calcium channel blockers (CCBs), the two major classes of antihypertensive drugs. Moreover, the majority of studies are based on randomized controlled trials and traditional meta-analyses, with few exploring the efficacy and safety comparisons among various members of ACEIs and CCBs. METHODS: ACEIs and CCB were searched for in randomized controlled trials in CNKI, Wanfang, VIP, China Biology Medicine Disc (Si-noMed), PubMed, EMbase, and Cochrane Library databases. The search can be conducted till November 2022. Stata software (version 16.0) and R 4.1.3 was used for statistical analysis and graphics plotting, applying mvmeta, gemtc, and its packages. Meta-regression analysis was used to explore the inconsistencies of the studies. RESULTS: In 73 trials involving 33 different drugs, a total of 9176 hypertensive patients were included in the analysis, with 4623 in the intervention group and 4553 in the control group. The results of the analysis showed that, according to the SUCRA ranking, felodipine (MD = -12.34, 95% CI: -17.8 to -6.82) was the drug most likely to be the best intervention for systolic blood pressure, while nitrendipine (MD = -8.01, 95% CI: -11.71 to -4.18) was the drug most likely to be the best intervention for diastolic blood pressure. Regarding adverse drug reactions, nifedipine (OR = 0.32, 95% CI: 0.14-0.74) was the drug most likely to be the safest. CONCLUSION: The research findings indicate that nifedipine is the optimal intervention for reducing systolic blood pressure in hypertensive patients, nitrendipine is the optimal intervention for reducing diastolic blood pressure in hypertensive patients, and felodipine is the optimal intervention for safety.

Qishen Yiqi dropping pills improve cardiomyocyte hypertrophy via the lncRNA TINCR/miR-193b-3p/RORA axis.

Background: This study was designed to explore the therapeutic effect and mechanism of action of Qishen Yiqi dropping pills (QYDP) in chronic heart failure (CHF) via a long non-coding RNA (lncRNA)-microRNA (miRNA)-messenger RNA (mRNA) axis. Here, the mechanism of action of the lncRNA terminal differentiation-induced non-coding RNA (TINCR), miR-193b-3p, and RAR-related orphan receptor A (RORA) mRNA was analyzed in an angiotensin (Ang) II-induced H9C2 cardiomyocyte hypertrophy model treated with QYDP. Methods: Reverse transcription-quantitative polymerase chain reaction (RT-qPCR) was used to analyze the gene expression changes of lncRNA, miRNA, and mRNA in H9C2 induced by QYDP on Ang II. The Gene Expression Omnibus (GEO) was used to analyze differentially expressed genes (DEGs) potentially affecting CHF progression. Cell Counting Kit-8 (CCK-8) was used to analyze the effect of QYDP on the proliferation of H9C2, RNA pull-down was used to analyze the binding of lncRNA and miRNA, and dual luciferase was used to analyze the targeting of miRNA and lncRNA or mRNA. Results: Ang II induced TINCR and RORA downregulation, miR-193b-3p upregulation, and hypertrophy in the H9C2 cardiomyocytes, which were alleviated by QYDP. In contrast, TINCR inhibition reversed the effects of QYDP by increasing miR-193b-3p expression and downregulating RORA expression. According to subsequent double luciferase and RNA pull-down experiments, TINCR adsorbed miR-193b-3p by acting as a competitive endogenous RNA sponge and miR-193b-3p directly targeted RORA. Lastly, we showed that the Ang-II-induced inhibition of TINCR and RORA expression and promotion of cardiac hypertrophy were both reversed by a TINCR overexpression plasmid (ov-TINCR), whereas the effects of ov-TINCR were suppressed by a miR-193b-3p mimic. Conclusions: Administration of QYDP improves Ang II-induced H9C2 cardiomyocyte hypertrophy and increase cell proliferation rate through the TINCR/miR-193b-3p/RORA axis.

The association between apolipoprotein E and gallstone disease: an updated meta-analysis.

BACKGROUND: Gallstone disease (GSD) is a common biliary tract disease worldwide. Previous studies have investigated the association of apolipoprotein E (APOE) E4 with GSD and reported inconsistent results. METHODS: In this paper, we conducted meta-analyses to examine whether APOE E4 is associated with the risk of GSD. A systematic literature search was performed in PubMed, Cochrane Library, EMBASE, and Google Scholar using the following inclusion criteria: 1) Studies on human subjects; 2) subjects in the control group must undergo ultrasound GSD screening, and presence of GSD in the experiment group can be clearly determined, e.g., diagnosis of GSD through ultrasound screening or a previous history of cholecystectomy or cholelithiasis; 3) the studies reported APOE genotype data (APOE E4+ vs. E4-) for subjects with and without GSD. In all the meta-analyses, we used random-effects models to calculate the odds ratios (ORs) as a measure of association as well as the corresponding confidence intervals (CIs). RESULTS: Our literature search found 13 publications with 14 studies, including a total of 1632 GSD patients and 5001 controls, that met the eligibility criteria and were included in the meta-analyses. We did not find a significant association between APOE E4 and risk of GSD (OR = 1.23, 95% CI: 0.89-1.68; p = 0.205). No significant associations were observed in subgroup analyses by gender and mean age. We obtained similar insignificant findings if an additive model was used, if subjects who had E2E4 genotype were excluded, or if low-quality studies were excluded. CONCLUSION: Our meta-analysis found insufficient evidence for the effect of APOE E4 on GSD risk. Future studies with large sample sizes that control for important confounding/risk factors are needed to validate our findings and to explore other genetic loci that might affect GSD risk.