Clinical and Experimental Hypertension最新文献

Objective: The concurrent prevalence of major depression and hypertension represents a significant clinical concern. This study aims to investigate the potential causal relationship among these conditions from a genetic standpoint.

Methods: The genome-wide association studies (GWAS) summary data for major depression were obtained from the IEU OpenGWAS database. Concurrently, GWAS summary data for hypertension were sourced from the Finnish consortium. All the participants have European ancestry. A two-sample bidirectional Mendelian randomization (MR) study was conducted to examine the relationship between major depression and hypertension. To ensure the reliability of the results, several sensitivity analyses were performed, addressing heterogeneity, horizontal pleiotropy, outliers, the influence of individual single nucleotide polymorphisms (SNPs), and adherence to normal distribution assumptions.

Results: The findings revealed a significant positive genetic causal association between major depression and hypertension (P = 0.016, odds ratio [OR] = 1.160, 95% confidence interval [CI] = 1.029-1.308). Conversely, no genetic causal relationship was identified between hypertension and major depression (P = 0.670, OR = 1.004, 95% CI = 0.985-1.024). Our MR analysis indicated the absence of heterogeneity and horizontal pleiotropy, with no detected outliers. Additionally, the analysis was not influenced by any SNP and demonstrated a normal distribution.

Conclusion: The results of this study indicate that severe depression is a risk factor for hypertension of European ancestry. The conclusion of this study should be used with caution when applied to other populations. Clinically depressed patients should be closely monitored for the onset of hypertension.

Background: Psychological problems such as anxiety and depression in children show an increasing prevalence, but low treatment rates and few interventions have been implemented. The relationship between combined exercise and psychological interventions on anxiety, depression, and blood pressure in children has not been clearly studied. The aim of this study was to investigate the effects of a combined psychological and exercise intervention program on children's anxiety and depression conditions and blood pressure.

Methods: Thirty-nine children aged 8-15 years from a middle school in Xishui County were included in a randomized controlled trial (18 in the intervention group and 21 in the control group). Physical examinations, such as blood pressure and questionnaires on anxiety/depression and quality of life, were collected. The intervention group underwent 7 days of continuous comprehensive motor‒psychological intervention.

Results: The Self-rating Anxiety Scale(SAS) in the intervention group decreased by 11.47 ± 7.99, which is higher than the control group decreased by 5.00 ± 10.22. The difference was statistically significant (P < 0.05). The self-rated depression scale (SDS) of the intervention group decreased from 58.80 ± 6.97 to 51.73 ± 5.76, with a statistically significant difference (P <0.05).The intervention activities also had a significant effect on the children's QoL indicators of companionship, living convenience, and living environment factor (all p ≤ 0.05). The intervention activities decreased the blood pressure and BMI of the children with statistically significant differences (p < 0.05).

Conclusion: The comprehensive intervention combining exercise and psychology domonstrated an effective approach to improve anxiety-depression status and blood pressure in adolescents and children, with a positive impact on quality of life.

Background: Transcatheter adrenal artery embolization (TAAE) has emerged as a minimally invasive technique for selective adrenal ablation, offering potential therapeutic applications for various adrenal disorders. However, its safety profile remains insufficiently characterized. This preclinical study aimed to evaluate the physiological, biochemical, and histological effects of ethanol-based TAAE in a large-animal model.

Methods: Twelve Bama miniature pigs were randomized into embolization (n = 6) and sham (n = 6) groups. The embolization group underwent selective unilateral adrenal artery embolization with absolute ethanol, while the sham group received catheterization without ethanol injection. Hemodynamic parameters, plasma adrenal hormones, renal function, and cardiac function were assessed preoperatively, intraoperatively, and at 4 weeks post-procedure. Histological analysis of adrenal tissues was performed to evaluate ablation effects.

Results: TAAE induced a transient but significant rise in systolic blood pressure (from 128 ± 11 to 219 ± 13 mmHg, P < 0.01) and plasma norepinephrine levels (from 7.4 ± 0.8 to 1199 ± 247 nmol/dL, P < 0.01) during ethanol injection, which normalized by 4 weeks. No significant differences were observed in body weight, renal function, serum electrolytes, adrenal hormone levels, or echocardiographic parameters at follow-up. Histological analysis revealed localized adrenal cortical necrosis, architectural disruption, and increased interstitial fibrosis in the embolization group (P < 0.01), without evidence of systemic toxicity or off-target embolization.

Conclusion: TAAE is a feasible and well-tolerated method for targeted adrenal ablation in a porcine model. This study provides foundational preclinical evidence supporting further investigation of TAAE as a minimally invasive, organ-sparing approach for the treatment of diverse adrenal pathologies.

This study was designed to elucidate the role of circPcmtd1 in regulating pulmonary artery smooth muscle cells (PASMCs) proliferation and migration, through the HSP90AB1/AKT signaling axis, in rats with high pulmonary blood flow-induced PAH. A rat model of high pulmonary blood flow-induced PAH was established by an abdominal aorta-inferior vena cava shunt surgery. The expression of circPcmtd1 in PASMCs of rats with high pulmonary blood flow-induced PAH was verified by qRT-PCR. The effects of circPcmtd1 on the proliferation and migration of PASMCs were explored by lentiviral transfection, cell proliferation assay, and scratch assay. RNA pull-down assay, mass spectrometric analysis, lentiviral transfection, and western blot were used to explore the molecular mechanisms by which circPcmtd1 regulated the proliferation and migration of PASMCs in rats with high pulmonary blood flow-induced PAH. We found that the expression of circPcmtd1 was down-regulated in PASMCs of rats with high pulmonary blood flow-induced PAH. Functional experiments showed that overexpression of circPcmtd1 inhibited the proliferation and migration of PASMCs. RNA pull-down assay and mass spectrometric analysis revealed that circPcmtd1 could bind to HSP90AB1 protein. Further, we found that high expression of HSP90AB1 could promote the proliferation and migration of PASMCs in rats with high pulmonary blood flow-induced PAH. Mechanistic investigation demonstrated that the binding of circPcmtd1 to HSP90AB1 could regulate the phosphorylation of AKT. In conclusion, circPcmtd1 directly bound to the HSP90AB1 protein to mediate the phosphorylation of AKT, thereby regulating the proliferation and migration of PASMCs.

Objective: This study aimed to investigate the prevalence of hypertension among young adults with MAFLD, assess the association between the presence and severity of MAFLD and hypertension, and explore potential mediating mechanisms linking MAFLD and hypertension in this population.

Methods: A total of 5,327 individuals aged 18-45 years from the National Health and Nutrition Examination Survey (2017-2023) were included. Multivariable logistic regression analysis was performed to evaluate the independent associations of MAFLD and its severity with hypertension and isolated diastolic hypertension. Mediation analysis assessed the mediating effects of inflammatory markers, including white blood cell (WBC) count, neutrophil count, and systemic immune-inflammation index (SII).

Results: The prevalence of MAFLD in the study population was 44.05%. Hypertension prevalence in the MAFLD group was significantly higher than in the non-MAFLD group (37.68% vs. 15.19%, P < 0.001). After adjusting for sex, age, race, alcohol consumption, and comorbidities such as diabetes and renal insufficiency, individuals with MAFLD and moderate-to-severe fibrosis exhibited a significantly higher risk of hypertension compared to non-MAFLD individuals (OR = 3.414, 95% CI: 2.522-4.622), P < 0.001). Mediation analysis demonstrated that WBC, neutrophils, and SII mediated 7.62% (95% CI: 2.75-15.00), 6.71% (95% CI: 2.48-12.65), and 5.90% (95% CI: 2.40-10.88) of the association between MAFLD and hypertension, respectively.

Conclusion: MAFLD, particularly in the presence of advanced liver fibrosis, is strongly and independently associated with hypertension in young adults. Systemic inflammation acts as a key mediator in this relationship, highlighting its potential as a therapeutic target for precision antihypertensive strategies in this population.

Pulmonary arterial hypertension (PAH) is a group of complex vasculopathies characterized by increased pulmonary arterial pressure and subsequent pulmonary vascular remodeling. However, the underlying pathogenesis of PAH has not been fully elucidated. In the present study, we employed bioinformatics technology to investigate the pathogenesis of PAH. Microarray datasets related to PAH were retrieved from the Gene Expression Omnibus database to screen for ER stress-related genes (ERSRGs) between normal control and PAH samples. The differentially expressed genes (DEGs) were analyzed for functional enrichment and protein‒protein interaction (PPI) networks. DEG-related miRNAs and transcriptional factor (TF) were predicted to construct the miRNA-TF-hub gene network. The diagnostic accuracy of the hub genes was assessed via receiver operating characteristic (ROC) curve analysis. The relative abundances of different types of immune cells were determined via immune infiltration analysis. The screening detected 20 ERSRGs between normal and PAH samples, nine of which (HIF1A, BCL2L1, TLR4, HMOX1, VCAM1, EGR1, MAPK8, LCN2, and CEBPB) were further identified as hub genes via the PPI network. To construct a regulatory network analysis of the Hub genes, 57 miRNAs and 35 TFs were subsequently predicted. There was a significant difference in the infiltration of 17 types of immune cells between the two groups. These results suggest that the nine hub genes might play crucial roles in the development of PAH. These findings might provide new therapeutic targets for PAH or potential biomarkers for its diagnosis.

With rapid advancements in genomics, proteomics, and metabolomics researchers have gained significant insights into ACS (ACS) pathogenesis. Studies have revealed specific biomarkers linked to ACS and provided novel tools for risk evaluation and early diagnosis. Genomic breakthroughs have enabled exploration of genetic factors contributing to ACS. Transcriptomics has facilitated the analysis of gene expression alterations in patients with ACS. Proteomics has identified potential therapeutic targets by pinpointing biomarkers, paving the way for new drug development. Advances in metabolomics have enabled monitoring of changes in metabolic pathways, offering valuable information for early diagnosis and disease prognosis. In summary, multiomics research has shed light on the critical aspects of ACS clinical strategies, facilitating advancements in early diagnosis, risk assessment, and personalized therapy, and will increasingly assume a pivotal role in future clinical practice.

Our previous study has found that miPEP31, which is encoded by pri-miRNA-31, inhibits the transcription of pri-miRNA-31 and alleviates angiotensin (Ang) II-induced hypertension. miR-31 is involved in proliferation of primary vascular smooth muscle cells (VSMCs), the key functional cells involved in hypertensive vascular remodeling. However, the role and mechanism of miPEP31 in the proliferation of VSMCs remain unclear. The aim of this study is to investigate whether miPEP31 plays an important role in VSMC proliferation and contributes to vascular remodeling. We found that the administration of synthetic miPEP31 mitigated but miPEP31 deficiency aggravated the Ang II-induced aortic thickness of intima plus media and fibrotic area. miPEP31 is endogenously expressed and penetrates into nuclei in VSMCs. miPEP31 inhibits PDGF-BB-induced VSMC proliferation in a dose-dependent manner and decreases the Ang Ⅱ-induced aortic α-SMA staining area. Mechanistically, we demonstrated that miPEP31 acts as a transcriptional repressor and inhibits miR-31 expression by cooperating with Trps1, a GATA family zinc finger transcription factor. In summary, our study suggests that miPEP31 protects against vascular remodeling in Ang II-infused mice via cooperation with transcription factor Trps1 to inhibit miR-31 expression and, subsequently, VSMC proliferation. This finding highlights the therapeutic effect and role of miPEP31 on hypertensive target organs and functional cells.

Objective: To evaluate the clinical utility of non-invasive hemodynamic indicators in assessing cardiovascular risk among hypertensive patients with coronary atherosclerotic heart disease (CAD), and to explore their correlation with lipid metabolism disorders.

Methods: A cross-sectional study was conducted on 598 hypertensive patients (312 hypertension-only vs. 286 hypertension-CAD). Participants underwent non-invasive hemodynamic monitoring (BioZ-Standard device) and lipid profiling. Group comparisons were performed using t-tests, and Pearson correlation was used to analyze associations between hemodynamics, lipids, and CAD. Receiver operating characteristic (ROC) curve analysis was used to assess diagnostic utility.

Results: The combined group demonstrated significantly impaired hemodynamic function compared to the hypertension-only group, with a lower CO (3.41 ± 0.45 vs 4.38 ± 0.51 L/min), SV (44.09 ± 4.38 vs 50.91 ± 4.63 mL), and CI (1.94 ± 0.25 vs 2.49 ± 0.29 L min^-1 m^-2) (all p < 0.001). Lipid profiles were markedly worse in patients with CAD, showing higher TC (4.76 ± 0.34 vs 4.35 ± 0.31 mmol/L) and LDL-C (3.32 ± 0.39 vs 2.89 ± 0.42 mmol/L) and lower HDL-C (1.09 ± 0.21 vs 1.23 ± 0.19 mmol/L) (all p < 0.001). Strong negative correlations were detected between the hemodynamic parameters and CAD status (CO: r = -0.672, p < 0.001; SV: r = -0.589, p < 0.001), and positive correlations were detected between dyslipidemia and CAD (LDL-C: r = 0.458, p < 0.001; HDL-C: r = -0.381, p < 0.001).

Conclusion: Non-invasive hemodynamic monitoring, particularly the measurement of CO and SV, combined with lipid profiling, offers quantitative markers for risk stratification in hypertensive patients. The significant correlations and diagnostic potential indicated by ROC analysis (AUC > 0.75 for key parameters) suggest that these measures can aid in the early detection and management of CAD in this high-risk population.

This retrospective cohort study assessed the predictive value of routine clinical indicators for diabetic nephropathy (DN) in elderly patients (≥60 years) with type 2 diabetes mellitus (T2DM) and hypertension. A total of 102 hospitalized patients (January 2022-December 2023) were divided into DN and non-DN groups. Fasting blood glucose (FBG), 2-h postprandial glucose (2hPG), HbA1c, systolic blood pressure (SBP), urinary microalbumin (UMA), and urinary albumin-to-creatinine ratio (UACR) were analyzed using univariate and multivariate logistic regression to identify independent predictors. A nomogram based on these indicators was developed and evaluated by receiver operating characteristic (ROC) analysis. All six factors independently predicted DN (p < 0.05), with 2hPG showing the strongest association (OR = 8.922). The combined model achieved high predictive accuracy (AUC = 0.906), outperforming any single indicator. This model offers a practical tool for early DN risk stratification in elderly T2DM patients with hypertension, supporting individualized prevention and intervention.