Clinical and Experimental Hypertension最新文献

{"title":"Efficacy and safety of intensive blood pressure control in patients over 60 years: A systematic review and meta-analysis.","authors":"Huarong Yang, Haiyan Xing, Xue Zou, Meihua Jin, Yang Li, Ke Xiao, Li Cai, Yao Liu, Xue Yang","doi":"10.1080/10641963.2025.2465399","DOIUrl":"10.1080/10641963.2025.2465399","url":null,"abstract":"<p><strong>Objectives: </strong>To evaluate the efficacy and safety of intensive blood pressure control in patients over 60 years.</p><p><strong>Methods: </strong>Databases including PubMed, Embase and Cochrane library were searched from inception through February 1, 2024. Randomized controlled trials evaluating the efficacy or safety of intensive blood pressure control in patients over 60 years were included in the meta-analysis.</p><p><strong>Results: </strong>Intensive blood pressure control in individuals with mild hypertension has been shown to reduce the risk of heart failure, stroke, myocardial infarction, major cardiovascular events, cardiovascular mortality, and all-cause mortality. The benefits of intensive blood pressure control in patients with moderate to severe hypertension are comparable to those observed in individuals with mild hypertension, with the exception of a reduced impact on all-cause mortality and cardiovascular mortality. Compared with maintaining systolic blood pressure (SBP) above 140 mmHg, SBP below 140 mmHg is associated with a decreased risk of major cardiovascular events in patients aged over 70, as well as a reduced risk of stroke in patients aged 60-69. Furthermore, compared to maintaining SBP above 130 mmHg, SBP below 130 mmHg is linked to a lower risk of major cardiovascular events, heart failure and myocardial infarction in patients over 60, a reduced risk of stroke and cardiovascular mortality in patients aged 60-69, and a decreased risk of all-cause mortality in patients over 70. However, a lower baseline blood pressure or more aggressive blood pressure control may be associated with an increased risk of hypotension.</p><p><strong>Conclusions: </strong>Patients with hypertension aged over 60 years can derive benefits from intensive blood pressure management without experiencing significant adverse events, aside from hypotension.</p>","PeriodicalId":10333,"journal":{"name":"Clinical and Experimental Hypertension","volume":"47 1","pages":"2465399"},"PeriodicalIF":1.5,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143413677","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":"Restoration of vascular dysfunction resulting from maternal high-fat diet via modulation of the NLRP3/IL-1β axis.","authors":"Yuxuan Xiao, Xianru Bi, Rongjie Zhang, Yu Li, Wei Sun, Yingxue Hao","doi":"10.1080/10641963.2024.2440342","DOIUrl":"https://doi.org/10.1080/10641963.2024.2440342","url":null,"abstract":"<p><p>This study investigated the impact of maternal high-fat diet on vascular function and endothelial homeostasis in offspring. We found that offspring exposed to maternal high-fat diet exhibited elevated blood pressure, impaired abdominal aortic vascular function, and endothelial homeostasis imbalance. These changes were accompanied by increased levels of reactive oxygen species (ROS) and upregulation of pro-inflammatory cytokines (including IL-1β, TNF-α, IL-6, and IL-10). Treatment with NLRP3 or IL-1β inhibitors prevented the deterioration in vascular function, reduced endothelial NO production, and inflammation induced by maternal high-fat diet exposure compared to the control group. The findings suggest that during pregnancy, mitigating the vascular impairments in offspring induced by maternal high-fat diet can be achieved by inhibiting the NLRP3/IL-1β pathway.</p>","PeriodicalId":10333,"journal":{"name":"Clinical and Experimental Hypertension","volume":"47 1","pages":"2440342"},"PeriodicalIF":1.5,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142892657","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":"Machine learning-based analyses of contributing factors for the development of hypertension: a comparative study.","authors":"Marenao Tanaka, Yukinori Akiyama, Kazuma Mori, Itaru Hosaka, Keisuke Endo, Toshifumi Ogawa, Tatsuya Sato, Toru Suzuki, Toshiyuki Yano, Hirofumi Ohnishi, Nagisa Hanawa, Masato Furuhashi","doi":"10.1080/10641963.2025.2449613","DOIUrl":"https://doi.org/10.1080/10641963.2025.2449613","url":null,"abstract":"<p><strong>Objectives: </strong>Sufficient attention has not been given to machine learning (ML) models using longitudinal data for investigating important predictors of new onset of hypertension. We investigated the predictive ability of several ML models for the development of hypertension.</p><p><strong>Methods: </strong>A total of 15 965 Japanese participants (men/women: 9,466/6,499, mean age: 45 years) who received annual health examinations were randomly divided into a training group (70%, <i>n</i> = 11,175) and a test group (30%, <i>n</i> = 4,790). The predictive abilities of 58 candidates including fatty liver index (FLI), which is calculated by using body mass index, waist circumference and levels of γ-glutamyl transferase and triglycerides, were investigated by statistics analogous to the area under the curve (AUC) in receiver operating characteristic curve analyses using ML models including logistic regression, random forest, naïve Bayes, extreme gradient boosting and artificial neural network.</p><p><strong>Results: </strong>During a 10-year period (mean period: 6.1 years), 2,132 subjects (19.1%) in the training group and 917 subjects (19.1%) in the test group had new onset of hypertension. Among the 58 parameters, systolic blood pressure, age and FLI were identified as important candidates by random forest feature selection with 10-fold cross-validation. The AUCs of ML models were 0.765-0.825, and discriminatory capacity was significantly improved in the artificial neural network model compared to that in the logistic regression model.</p><p><strong>Conclusions: </strong>The development of hypertension can be simply and accurately predicted by each ML model using systolic blood pressure, age and FLI as selected features. By building multiple ML models, more practical prediction might be possible.</p>","PeriodicalId":10333,"journal":{"name":"Clinical and Experimental Hypertension","volume":"47 1","pages":"2449613"},"PeriodicalIF":1.5,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142945761","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":"Cinnamaldehyde alleviates pulmonary hypertension by affecting vascular remodeling through the TLR4/NF-kB/HIF-1a pathway.","authors":"Jinbo Zhang, Wenxin Zhang, Zhiyong Yang, Bingbing Fan, Chunhe Wang, Zhengkun Tian","doi":"10.1080/10641963.2025.2486829","DOIUrl":"10.1080/10641963.2025.2486829","url":null,"abstract":"<p><strong>Objective: </strong>To investigate the mechanism by which cinnamaldehyde (CA) alleviates pulmonary arterial hypertension (PAH) through the TLR4/NF-kB/HIF-1a pathway.</p><p><strong>Methods: </strong>PAH was induced in rats via SU5416 injection and hypoxia. Hemodynamics (RVMP, RVSP, mPAP) were measured. Histological changes were assessed by HE staining, and protein expressions of α-SMA, Col I, TLR4, p-p65, p65, and HIF-1a were detected by western blot. In vitro, hypoxia-induced HPAECs were treated with CA and TLR4 activator RS09TFA. Cell function was assessed by CCK-8, colony formation, and scratch assays, with VE-Cadherin and α-SMA expression analyzed by western blot.</p><p><strong>Results: </strong>PAH rats showed increased RVMP, RVSP, mPAP, and pulmonary artery thickening. CA significantly alleviated lung damage and reduced α-SMA and Col I expression. TLR4/NF-kB/HIF-1a activation with RS09TFA inhibited CA's effects. In vitro, CA mitigated hypoxia-induced HPAEC dysfunction, restoring VE-Cadherin and α-SMA expression, while RS09TFA blocked these effects.</p><p><strong>Conclusion: </strong>CA alleviates PAH by inhibiting the TLR4/NF-kB/HIF-1a pathway and suppressing vascular remodeling, suggesting its potential as a therapeutic agent for PAH.</p>","PeriodicalId":10333,"journal":{"name":"Clinical and Experimental Hypertension","volume":"47 1","pages":"2486829"},"PeriodicalIF":1.5,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143763207","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":"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":"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":"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}