Clinical and Experimental Hypertension最新文献

{"title":"Relationship between lipoprotein B and the severity of coronary microvascular dysfunction.","authors":"Lili Yang, Jingjing Zhang, Jiangyan Han, Xiaojuan Jiang","doi":"10.1080/10641963.2025.2477651","DOIUrl":"10.1080/10641963.2025.2477651","url":null,"abstract":"<p><strong>Objective: </strong>Contributing factors for the development of heart failure (HF) involve both apolipoprotein B (ApoB) and coronary microvascular dysfunction (CMD). Although ApoB has been linked to diverse cardiovascular risks, its association with CMD remains unclear.</p><p><strong>Methods: </strong>A total of 145 patients undergoing cardiac single-photon emission computed tomography (SPECT) scan was enrolled into this retrospective study. Based on ApoB serum level, all subjects were classified into three groups (Group 1-3). Myocardial flow reserve (MFR) was calculated using myocardial blood flow (MBF) tested in different contexts.</p><p><strong>Results: </strong>ApoB serum level was positively correlated to rest MBF but inversely associated with stress MBF and MFR. Following adjustment for covariates, a significant relationship was observed between increased ApoB and decreased MFR. The predictive value of ApoB was test by Receiver Operating Characteristic Curve (ROC) analysis, showing an area under curve (AUC) of 0.87.</p><p><strong>Conclusion: </strong>The findings indicated that a higher level of ApoB correlated with the severity of CMD.</p>","PeriodicalId":10333,"journal":{"name":"Clinical and Experimental Hypertension","volume":"47 1","pages":"2477651"},"PeriodicalIF":1.5,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143656250","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Establishment of a lupus-prone mouse model of pulmonary arterial hypertension with intermittent hypoxia: functional, biochemical and histological verifications.","authors":"Dengfeng Wu, Jiangbiao Xiong, Yiping Huang, Yue Yuan, Shunjia Xing, Rui Wu","doi":"10.1080/10641963.2025.2500383","DOIUrl":"https://doi.org/10.1080/10641963.2025.2500383","url":null,"abstract":"<p><p>Pulmonary arterial hypertension (PAH) is one of the most severe complications of systemic lupus erythematosus (SLE) with high mortality and limited treatment options, primarily due to its unclear pathogenesis. This study aims to investigate the role of intermittent hypoxia (IH) in exacerbating pulmonary arterial remodeling in SLE-PAH using MRL/lpr lupus-prone mouse. In this study, twelve female MRL/lpr mice and six female BALB/c mice were exposed to hypoxia for 2 hours daily over 28 days in a hypoxic chamber (FiO₂, 12%). Among them, six MRL/lpr mice received treatment with LW6, a HIF-1α inhibitor. Moreover, six MRL/lpr mice were exposed to normoxia (FiO2, 21%) and served as controls. As a result, IH MRL/lpr mice developed significant PAH, with right ventricular systolic pressure (RVSP) measuring 32.95 ± 2.08 mmHg, significantly higher than the 26.63 ± 2.72 mmHg observed in normoxic MRL/lpr mice (<i>p</i> < .001). Additionally, the right ventricular hypertrophy index (RVHI) and medial wall thickness (MWT) of pulmonary artery markedly elevated in IH MRL/lpr mice. The protein expression level of HIF-1a and P-NFκB were significantly upregulated in the lungs of these mice. However, treatment with LW6 during hypoxia reduced RVSP and alleviated pulmonary arterial remodeling in MRL/lpr mice. Notably, BALB/c mice subjected to 2 hours of daily hypoxia did not exhibit pulmonary arterial remodeling. This study establishes a reproducible SLE-PAH model, demonstrates the critical role of hypoxia in disease progression, and identifies HIF-1α as a potential therapeutic target for managing SLE-PAH.</p>","PeriodicalId":10333,"journal":{"name":"Clinical and Experimental Hypertension","volume":"47 1","pages":"2500383"},"PeriodicalIF":1.5,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143983477","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correction.","authors":"","doi":"10.1080/10641963.2025.2496584","DOIUrl":"https://doi.org/10.1080/10641963.2025.2496584","url":null,"abstract":"","PeriodicalId":10333,"journal":{"name":"Clinical and Experimental Hypertension","volume":"47 1","pages":"2496584"},"PeriodicalIF":1.5,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143975430","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Serum uric acid levels as a causal factor in hypertension: Insights from Mendelian randomization analysis.","authors":"Jiayue Xu, Jiajing Zhao, Jiaming Gu, Wenjian Wang, Jingxian Chen","doi":"10.1080/10641963.2025.2496514","DOIUrl":"https://doi.org/10.1080/10641963.2025.2496514","url":null,"abstract":"<p><strong>Background: </strong>Hyperuricemia and hypertension are prevalent chronic diseases that often co-occur. While numerous observational studies suggest an association between serum uric acid (SUA) levels and hypertension, the causal nature of this relationship remains unresolved due to confounding and reverse causation. This study systematically investigates the causal association between SUA levels and hypertension risk using Mendelian randomization (MR) methodologies.</p><p><strong>Methods: </strong>We utilized single nucleotide polymorphisms (SNPs) identified in large-scale genome-wide association studies (GWAS) of European populations as genetic instruments for SUA levels. MR, a genetic epidemiology technique, uses genetic variations as proxies to mimic a randomized controlled trial and minimizing biases from confounding and reverse causation. Systolic and diastolic blood pressure (SBP and DBP) were the primary outcomes of interest. A two-sample MR analysis was conducted to assess the causal relationships, complemented by sensitivity analyses (weighted median, weighted mode, MR-Egger) to ensure result robustness. Findings are expressed as odds ratios (ORs) with 95% confidence intervals (Cis) per one standard deviation (SD) increase in SUA levels.</p><p><strong>Results: </strong>Our MR analysis identified a significant causal effect of SUA levels on hypertension risk. Specifically, genetically predicted SUA levels were positively associated with SBP (β = 0.136 [0.035-0.238], <i>p</i> < .05) and DBP (β = 0.108 [0.007-0.209], <i>p</i> < .05).Conversely, reverse MR analysis revealed no significant causal effect of SBP (b = 0.058 [ - 9.52E-05-0.116],<i>p</i> = .0504] or DBP (β = 0.016 [ - 0.028-0.059], <i>p</i> > .05] on SUA levels, confirming the unidirectional nature of this association.</p><p><strong>Conclusion: </strong>This study provides compelling evidence from MR supporting a unidirectional causal link between SUA levels and increased hypertension risk. Unlike prior observational studies, our genetic approach effectively mitigates confounding and reverse causation, offering novel insights into the etiology of hypertension. These findings highlight the clinical importance of managing SUA levels to mitigate hypertension risk. Further research, including randomized controlled trials, is needed to confirm these findings and explore potential therapeutic interventions targeting SUA.</p>","PeriodicalId":10333,"journal":{"name":"Clinical and Experimental Hypertension","volume":"47 1","pages":"2496514"},"PeriodicalIF":1.5,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143975431","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Lycopene attenuates trimethylamine-N-oxide-induced senescence in endothelial progenitor cells via the AMPK/SIRT1 pathway.","authors":"Yanfeng Liu, Zhenhao Liu, Tengcan Tu, Hao Liu, Chujun Tan, Dan Feng, Jun Zou","doi":"10.1080/10641963.2025.2487891","DOIUrl":"10.1080/10641963.2025.2487891","url":null,"abstract":"<p><p>Aging-related diseases, which are associated with the senescence of endothelial progenitor cells (EPCs), are consistently accompanied by elevated levels of circulating trimethylamine-N-oxide (TMAO), a marker predictive of poor prognosis. Lycopene (Lyc) deficiency has been demonstrated to be linked to these age-related diseases. The AMPK/SIRT1 pathway plays a pivotal role in cellular senescence. In this study, we hypothesize that lycopene could mitigate TMAO-induced EPCs senescence, with involvement of the AMPK/SIRT1 pathway. EPCs were subjected to treatment with TMAO, Lyc, small interfering RNA targeting AMP-activated protein kinase (siAMPK), or sirtin-1 (siSIRT1). The biological functions of EPCs were evaluated through, CCK-8, transwell and tube formation assays, while their senescence was assessed via SA-β-gal activity assay and Western blotting. ROS generation was measured using dichlorodihydrofluorescein diacetate staining. TMAO-induced suppression of EPCs' functionality was alleviated by Lyc, but this effect was reversed by siAMPK and siSIRT1. TMAO increased SA-β-gal-positive cell number and ROS production, while reducing the expression of AMPK and SIRT1. These effects were attenuated by Lyc. However, the protective effects were diminished by siAMPK and siSIRT1. In conclusion, Lyc ameliorates TMAO-induced EPCs senescence through the AMPK/SIRT1 pathway.</p>","PeriodicalId":10333,"journal":{"name":"Clinical and Experimental Hypertension","volume":"47 1","pages":"2487891"},"PeriodicalIF":1.5,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143794865","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correction.","authors":"","doi":"10.1080/10641963.2025.2499376","DOIUrl":"https://doi.org/10.1080/10641963.2025.2499376","url":null,"abstract":"","PeriodicalId":10333,"journal":{"name":"Clinical and Experimental Hypertension","volume":"47 1","pages":"2499376"},"PeriodicalIF":1.5,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143978222","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Anthocyanin attenuates pulmonary arterial hypertension and associated heart failure via improving mitochondrial function through Nrf2-dependent mechanism.","authors":"Xiao Liu, Xiaoli Tan, Yidan Su, Luohao Zou, Wenhui Yuan, Changqing Yu","doi":"10.1080/10641963.2025.2503805","DOIUrl":"https://doi.org/10.1080/10641963.2025.2503805","url":null,"abstract":"<p><strong>Background: </strong>Mitochondrial dysfunction of pulmonary vascular endothelial cells is one of the important pathogenesis of pulmonary arterial hypertension (PAH). Anthocyanin can protect mitochondrial function, but whether anthocyanin can prevent PAH and its related mechanism has not been reported.</p><p><strong>Methods: </strong>Using rodent PAH models induced by chronic hypoxia for 21 days, we investigated the changes of hemodynamics, histopathology and vascular endothelial function after anthocyanin treatment for 21 days.</p><p><strong>Results: </strong>We found that anthocyanin treatment improved pulmonary endothelial function, vascular remodeling and associated right heart failure. Mechanistically, we found that anthocyanin treatment promoted the nucleus translocation of Nrf2 and improved the impaired mitochondrial function. The beneficial effects of anthocyanin on regulation of mitochondrial function were abolished by inhibition of Nrf2. Finally, in Nrf2 deficient mice, the protective effects of anthocyanin on PAH were largely vanished.</p><p><strong>Conclusions: </strong>Collectively, we showed that anthocyanin attenuated PAH and associated right heart failure via improving mitochondrial function through Nrf2-dependent mechanism, suggesting that anthocyanin may represent a novel therapeutic potential for PAH.</p>","PeriodicalId":10333,"journal":{"name":"Clinical and Experimental Hypertension","volume":"47 1","pages":"2503805"},"PeriodicalIF":1.5,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143976391","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A clinical study of coronary computed tomographic angiography in the diagnostic performance, risk assessment and guidance of treatment for coronary heart disease.","authors":"Haijun Li, Yanan Xie, Shujun Wang, Daiwei Wang","doi":"10.1080/10641963.2025.2524104","DOIUrl":"10.1080/10641963.2025.2524104","url":null,"abstract":"<p><strong>Objective: </strong>This study aimed to evaluate the diagnostic performance, risk assessment, and treatment-guiding value of coronary computed tomographic angiography (CCTA) in patients with coronary heart disease (CHD).</p><p><strong>Methods: </strong>The diagnostic value of CCTA for CHD was assessed by analyzing key parameters including sensitivity, specificity, accuracy, positive predictive value, and negative predictive value. Additionally, the diagnostic relevance of specific CCTA-derived metrics was explored. Patients with confirmed CHD underwent percutaneous coronary intervention (PCI), and the occurrence of major adverse cardiovascular events (MACE) within one year after PCI were recorded. Differences in CCTA parameters between patients with and without MACE were compared. Multivariate logistic regression was conducted to identify independent risk factors for post-PCI MACE.</p><p><strong>Results: </strong>CCTA demonstrated high diagnostic value for CHD. Compared to the control group, patients with CHD exhibited significantly greater plaque length, total plaque volume, calcified plaque volume, lipid plaque volume, plaque burden, and coronary diameter stenosis, along with a smaller minimum lumen area. These imaging features were predictive of CHD. Relative to the non-MACE group (<i>n</i> = 69), the MACE group (<i>n</i> = 56) had higher plaque length, total plaque volume, plaque burden, and coronary diameter stenosis rate, and smaller minimum lumen area. Multivariate logistic regression analysis identified plaque burden, coronary diameter stenosis, and hypertension serve as independent predictors for adverse cardiovascular events following PCI in CHD patients.</p><p><strong>Conclusion: </strong>CCTA is a valuable noninvasive modality for the diagnosis of CHD, risk assessment, and optimization of treatment strategies, particularly in predicting adverse outcomes following PCI.</p>","PeriodicalId":10333,"journal":{"name":"Clinical and Experimental Hypertension","volume":"47 1","pages":"2524104"},"PeriodicalIF":1.5,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144474137","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Disruption of the caspase-1/IL-1β axis alleviates myocardial Ischemia/Reperfusion injury via improvement of mitochondrial homeostasis and reduction of Pyroptosis.","authors":"ChenKai Hu, FengXia Yuan, YingXing Wu, Shan Xiao, Yuan Xu, Xiang Peng, Lei He","doi":"10.1080/10641963.2025.2506619","DOIUrl":"https://doi.org/10.1080/10641963.2025.2506619","url":null,"abstract":"<p><strong>Background: </strong>Pyroptosis is a novel kind of programmed cell death and Caspase-1 plays key roles in driving pyroptosis. The current study aims to elucidate the molecular mechanism affecting cardiomyocyte pyroptosis in myocardial ischemia/reperfusion (I/R) injury, both in vivo and in vitro.</p><p><strong>Methods: </strong>A murine model of myocardial I/R injury was established and then treated with lentivirus-mediated shRNA targeting Caspase-1 to evaluate the effect of Caspase-1 on myocardial I/R injury. Further, Caspase-1 was silenced in the cardiomyocytes following hypoxia-reoxygenation (H/R) to detect the function of Caspase-1 in mitochondrial homeostasis and cardiomyocyte pyroptosis.</p><p><strong>Results: </strong>Knockdown of Caspase-1 inhibited the secretion of interleukin-1 beta (IL-1β), improved cardiac dysfunction and decreased pyroptosis in vivo. The cardio-protective effect was verified in the H/R-induced cardiomyocyte model. Recombinant IL-1β protein reversed the inhibitory effect of Caspase-1 knockdown on pyroptosis.</p><p><strong>Conclusion: </strong>Overall, activating the Caspase-1/IL-1β axis by myocardial I/R injury causes mitochondrial homeostasis imbalance, pyroptosis, and the consequent cardiomyocyte injury.</p>","PeriodicalId":10333,"journal":{"name":"Clinical and Experimental Hypertension","volume":"47 1","pages":"2506619"},"PeriodicalIF":1.5,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144076410","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mechanistic study of the association between microRNA-126 and hypertension in obstructive sleep apnea-hypopnea syndrome.","authors":"Xiaobo Huang, Wenjuan Hu, Lijun Chen, Liting Ma, Gengen Yu, Juanxia Chen, Huifang Zhang, Fan Cao, Huijie Wang","doi":"10.1080/10641963.2025.2511056","DOIUrl":"https://doi.org/10.1080/10641963.2025.2511056","url":null,"abstract":"<p><strong>Objective: </strong>This study explored miRNA-126 and HIF-1α levels in patients with OSAHS-related hypertension. To analyze the relationship between miRNA-126 and OSAHS-related hypertension and explore the pathogenic mechanisms of miRNA-126 and the HIF-1α pathway.</p><p><strong>Materials and methods: </strong>The 120 participants were assigned to four groups based on their apnea-hypopnea index (AHI) and the presence of hypertension: healthy control group, hypertension group, non-hypertensive OSAHS group, and OSAHS-related hypertension group, with 30 objects in each group. All subjects underwent overnight sleep monitoring and 24-hour (h) ambulatory blood pressure. Their blood samples were analyzed for the following parameters: triglycerides (TG), fasting blood glucose (GLU), total cholesterol (TC), HDL, uric acid (UA), and LDL, hypoxia-inducible factor-1 alpha (HIF-1α), VEGF, C-reactive protein (CRP), IL-6 and tumor necrosis factor alpha (TNF-α). The relative expression levels of miRNA-126 were assessed by RT-qPCR and Western blotting, and dual-luciferase reporter assays were conducted to verify the association between miR-126-3p and HIF1-α.</p><p><strong>Results: </strong>Results indicated that HIF-1α is a target gene of miRNA-126 and is negatively regulated by miRNA-126; Levels of miRNA-126 were significantly lower in OSAHS and hypertension patients relative to healthy controls, with the lowest levels observed in the OSAHS-related hypertension group(<i>p</i> < .05). miRNA-126 levels were negatively correlated with HIF-1α, VEGF, TNF-α, CRP, IL-6, TG, TC, LDL, GLU and UA levels (<i>p</i> < .01), while it showed positive correlation with HDL level (<i>p</i> < .01).</p><p><strong>Conclusion: </strong>The level of miRNA-126 in patients with OSAHS-related hypertension is lower than that in patients with OSAHS alone and those with hypertension alone.</p>","PeriodicalId":10333,"journal":{"name":"Clinical and Experimental Hypertension","volume":"47 1","pages":"2511056"},"PeriodicalIF":1.5,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144141869","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}