Hypertension induces both structural and functional changes in blood vessels, thereby increasing endothelial dysfunction, which in turn, contributes to an increase in blood pressure. A popular and widely used noninvasive tool, flow-mediated dilation (FMD), is used to examine peripheral artery endothelium-dependent dilation. This study aimed to compare the efficacies of different classes of antihypertensive agents based on their effects on FMD. PubMed, Embase, and Cochrane Library were queried till November 1, 2020. Comparative studies on the efficacies of two or more antihypertensive agents or placebos for hypertensive patients were included. The outcomes were variations in mean systolic and diastolic blood pressure. Two reviewers independently reviewed and filtered the literature and extracted the data; the Cochrane “risk of bias” method was used to evaluate the methodological quality of the randomized controlled trials. A network meta-analysis was performed using Stata 15.0 software with a total of 49 studies. Subgroup analysis based on age and duration of treatments was performed. As compared to the placebo group, patients receiving the antihypertensive drugs exhibited significantly enhanced FMD (ARB + CCB: 4.01%, 95% CI, 0.92–7.11%, p < 0.001 ; ACEI + ARB: 2.81%, 95% CI, 1.19–4.43%, p < 0.001 ; ACEI: 2.55%, 95% CI, 1.34–3.77%, p < 0.001 ; ARB: 2.22%, 95% CI, 1.05–3.38%, p < 0.001 ; β-blocker: 2.23%, 95% CI, 0.93–3.52%, p < 0.001 ). In the SUCRA curve for network meta-analysis, the combination of CCB and ARB was found to be the most effective in increasing FMD (SUCRA = 89.0%), followed by ACEI monotherapy (SUCRA = 74.2%). ARB combined with CCB was superior in improving the endothelial function measured as the FMD; ACEI monotherapy was the most effective treatment among the antihypertension medications. There were no significant differences between antihypertensive drug-based monotherapies.
Myocardial ischemia and hypoxia are one of the main causes of heart failure, and cardiomyocyte apoptosis induced by mitochondrial injury is the basis of poor heart remodeling and heart failure. Upstream stimulatory factor 2 (USF2), a transcription factor involved in multiple cellular processes, has recently been identified as having an active role in mitochondrial function and energy homeostasis; however, the role of USF2 in cardiovascular disease has not been reported. In this study, we demonstrated that the expression of USF2 protein can be degraded by the ubiquitin-proteasome pathway when cardiomyocytes are hypoxic, and the loss of USF2 can lead to mitochondrial dysfunction in cardiomyocytes, aggravating mitochondrial damage and further promoting apoptosis.Mechanistically, we also demonstrate that USF2 deficiency induces mitochondrial autophagy by [regulating](javascript:;) the AMPK/mTOR signaling pathway.Altogether, this study provides new insights into the protective role of USF2 in hypoxic cardiomyocyte injury. USF2 may serve as a potential therapeutic target for myocardial hypoxia.
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