Clinical and Experimental Hypertension最新文献

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The causal relationship between aspartate aminotransferase and hypertension: A bidirectional Mendelian randomization study. 天冬氨酸转氨酶与高血压的因果关系:一项双向孟德尔随机研究。
IF 3.5 4区 医学
Clinical and Experimental Hypertension Pub Date : 2025-12-31 Epub Date: 2025-10-05 DOI: 10.1080/10641963.2025.2564298
Hongyan Song, Jun Li, Lizhen Lan, Huaxing Meng
{"title":"The causal relationship between aspartate aminotransferase and hypertension: A bidirectional Mendelian randomization study.","authors":"Hongyan Song, Jun Li, Lizhen Lan, Huaxing Meng","doi":"10.1080/10641963.2025.2564298","DOIUrl":"https://doi.org/10.1080/10641963.2025.2564298","url":null,"abstract":"<p><strong>Background: </strong>Hypertension is a major contributor to the global burden of disease and increased mortality in the general population. Currently, the etiology and pathogenesis of hypertension are not fully understood. Emerging evidence suggests an association between aspartate aminotransferase (AST) and hypertension, but whether this relationship is causal remains unclear.</p><p><strong>Methods: </strong>A two-sample MR analysis was conducted using GWAS summary data. Five MR methods - MR-Egger, weighted median, inverse variance weighted (IVW), simple mode, and weighted mode - were applied, with IVW as the primary approach. Sensitivity analyses, including heterogeneity and pleiotropy assessments, as well as leave-one-out (LOO) analysis, were performed. Functional annotation of non-coding SNPs was conducted using the 3DSNP database, while GeneMania and enrichment analysis explored gene interactions and biological pathways.</p><p><strong>Results: </strong>Forward MR analysis using the IVW method indicated a significant causal effect of AST on hypertension (<i>β</i> = 0.0003, Standard Error (SE) = 6.93E-05, <i>P</i> = 0.0002). However, reverse MR analysis found no significant causal relationship between hypertension and AST (<i>β</i> = 15.7148, SE = 12.7551 <i>P</i> = 0.2179). The results of MR-Egger regression, Weighted Median, and Weighted Mode methods were consistent with those of the IVW method. These findings were robust across several reliability analyses. Finally, network and functional enrichment analyses showed that, under the influence of IVs, the SNP-hosted genes and AST promote disease progression through involvement in aspartic acid family metabolism and hexose biosynthesis.</p><p><strong>Conclusion: </strong>The present study reports the potential role of AST in the development of hypertension. The link between AST and hypertension may be due to regulation of substance and energy metabolism. These findings offer new insights into the pathophysiology of hypertension and suggest that AST could serve as a potential biomarker or therapeutic target for hypertension management.</p>","PeriodicalId":10333,"journal":{"name":"Clinical and Experimental Hypertension","volume":"47 1","pages":"2564298"},"PeriodicalIF":3.5,"publicationDate":"2025-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145231547","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}
引用次数: 0
Targeting the PHD2/HIF-1α/HO-1 pathway: A key role of trimetazidine in hypertensive nephropathy. 靶向PHD2/HIF-1α/HO-1通路:曲美他嗪在高血压肾病中的关键作用
IF 3.5 4区 医学
Clinical and Experimental Hypertension Pub Date : 2025-12-31 Epub Date: 2025-10-11 DOI: 10.1080/10641963.2025.2563033
Daqian Gu, Meixian Chen, Yuhui Yang, Chen Lu, Chao Li, Yi Lin
{"title":"Targeting the PHD2/HIF-1α/HO-1 pathway: A key role of trimetazidine in hypertensive nephropathy.","authors":"Daqian Gu, Meixian Chen, Yuhui Yang, Chen Lu, Chao Li, Yi Lin","doi":"10.1080/10641963.2025.2563033","DOIUrl":"https://doi.org/10.1080/10641963.2025.2563033","url":null,"abstract":"<p><strong>Objective: </strong>This study seeks to unravel the effects of trimetazidine (TMZ) on hypertensive nephropathy (HN) in mice and its underlying mechanisms.</p><p><strong>Methods: </strong>Sixty male 129 mice (8-10 weeks old) were randomly categorized into six groups (<i>n</i> = 10 per group): control, model, TMZ, TMZ + small interfering RNA targeting prolyl hydroxylase domain protein 2 (si-PHD2), TMZ + zinc protoporphyrin [ZnPP, a heme oxygenase-1 (HO-1) inhibitor], and TMZ + KC7F2 [a hypoxia-inducible factor-1 alpha (HIF-1α) inhibitor]. All groups except the control group received angiotensin II to induce HN models. TMZ was administered by gavage for 28 days, while the other TMZ-based groups received additional si-PHD2, ZnPP, or KC7F2. Blood pressure, renal function, proinflammatory cytokines, and kidney pathology were measured. Protein/mRNA levels of PHD2, HO-1, HIF-1α, and Collagen I were analyzed via reverse transcription quantitative polymerase chain reaction/Western blot.</p><p><strong>Results: </strong>The model group showed increased blood pressure, renal injury, fibrosis, and elevated levels of PHD2, HIF-1α, HO-1, Collagen I, and inflammatory markers compared to the control group (<i>P</i> < 0.05). TMZ treatment alleviated renal damage and downregulated PHD2, while upregulating HIF-1α and HO-1. These effects were further enhanced by PHD2 knockdown (TMZ + si-PHD2), but reversed by the inhibition of HO-1 or HIF-1α (TMZ + ZnPP, TMZ + KC7F2).</p><p><strong>Conclusion: </strong>TMZ improves HN in mice by modulating the PHD2/HIF-1α/HO-1 pathway.</p>","PeriodicalId":10333,"journal":{"name":"Clinical and Experimental Hypertension","volume":"47 1","pages":"2563033"},"PeriodicalIF":3.5,"publicationDate":"2025-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145273949","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}
引用次数: 0
Neuroprotective peptide OL-FS13 attenuates cardiac apoptosis and myocardial infarction injury through Nrf2/HO-1 pathway. 神经保护肽OL-FS13通过Nrf2/HO-1通路减轻心肌细胞凋亡和心肌梗死损伤。
IF 3.5 4区 医学
Clinical and Experimental Hypertension Pub Date : 2025-12-31 Epub Date: 2025-09-11 DOI: 10.1080/10641963.2025.2556422
Hao Wang, Ke Zhou, Xiaoling Chen, Yao Tong, Qiuyan Jiang, Qiang She, Jun Xiao
{"title":"Neuroprotective peptide OL-FS13 attenuates cardiac apoptosis and myocardial infarction injury through Nrf2/HO-1 pathway.","authors":"Hao Wang, Ke Zhou, Xiaoling Chen, Yao Tong, Qiuyan Jiang, Qiang She, Jun Xiao","doi":"10.1080/10641963.2025.2556422","DOIUrl":"https://doi.org/10.1080/10641963.2025.2556422","url":null,"abstract":"<p><p>Myocardial infarction (MI) is a leading cause of morbidity and mortality globally, primarily due to oxidative stress-induced cardiomyocyte apoptosis and adverse cardiac remodeling. OL-FS13, a neuroprotective peptide derived from Odorrana livida, has previously shown anti-apoptotic effects in cerebral ischemia models. However, its role in myocardial protection remains unclear. In this study, we investigated the cardioprotective effects of OL-FS13 in both in vitro and in vivo models of MI. Hydrogen peroxide (H₂O₂) was used to induce oxidative stress in primary neonatal rat cardiomyocytes, while permanent ligation of the left anterior descending (LAD) coronary artery was employed to establish a murine MI model. OL-FS13 treatment significantly attenuated cardiomyocyte apoptosis, reduced ROS accumulation, improved left ventricular function, and decreased infarct size. Mechanistically, OL-FS13 activated the Nrf2/HO-1 signaling pathway, restoring antioxidant protein levels and suppressing oxidative stress-induced apoptosis. Pharmacological inhibition of Nrf2 with ML385 abrogated the antioxidant and anti-apoptotic effects of OL-FS13 both in vitro and in vivo, confirming the central role of this pathway. These findings demonstrate that OL-FS13 exerts potent cardioprotective effects via Nrf2/HO-1 pathway activation and ROS suppression, suggesting its potential as a novel therapeutic agent for the treatment of myocardial infarction.</p>","PeriodicalId":10333,"journal":{"name":"Clinical and Experimental Hypertension","volume":"47 1","pages":"2556422"},"PeriodicalIF":3.5,"publicationDate":"2025-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145032915","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}
引用次数: 0
Hypertension accelerates aging: Evidence from NHANES database and Mendelian randomization analyses. 高血压加速衰老:来自NHANES数据库和孟德尔随机化分析的证据。
IF 3.5 4区 医学
Clinical and Experimental Hypertension Pub Date : 2025-12-31 Epub Date: 2025-09-17 DOI: 10.1080/10641963.2025.2559743
Zhaobin Sun, Gaoying Dai, Nanhu Quan
{"title":"Hypertension accelerates aging: Evidence from NHANES database and Mendelian randomization analyses.","authors":"Zhaobin Sun, Gaoying Dai, Nanhu Quan","doi":"10.1080/10641963.2025.2559743","DOIUrl":"https://doi.org/10.1080/10641963.2025.2559743","url":null,"abstract":"<p><strong>Background: </strong>Hypertension is thought to accelerate biological aging. However, evidence of a causal effect is lacking. This study aimed to provide evidence of a relationship between hypertension and biological aging by analyzing data from the 2005-2010 National Health and Nutrition Examination Survey (NHANES) and by Mendelian randomization (MR).</p><p><strong>Methods: </strong>The association of hypertension with PhenoAge and PhenoAge acceleration was assessed by weighted multivariable-adjusted linear regression using the NHANES data. Two-sample MR was then performed using summary data from genome-wide association studies to determine causal associations of hypertension with accelerated DNA methylation (DNAm) and proxies of age, including telomere length, frailty index, and facial aging. Inverse variance weighting and complementary MR methods were used to confirm the causal relationship between hypertension and biological aging. The robustness of the results was confirmed by sensitivity analyses.</p><p><strong>Results: </strong>Data for 6102 NHANES participants were analyzed. Weighted multivariable-adjusted linear regression analyses showed that hypertension increased PhenoAge (<i>β</i> = 12, 95% CI: 11-13, <i>p </i>< 0.001) and was positively associated with PhenoAge acceleration (<i>β</i> = 0.56, 95% CI: 0.15-0.98, <i>p</i> = 0.009). The MR results also suggested a potential causal association of hypertension with DNAm PhenoAge acceleration (OR 1.31, 95% CI: 1.07-1.60, <i>p </i>< 0.05), DNAm GrimAge acceleration (OR 1.33, 95% CI: 1.13-1.57, <i>p </i>< 0.05), and the frailty index (OR 1.09, 95% CI: 1.07-1.11, <i>p </i>< 0.05). Sensitivity analyses confirmed the robustness and reliability of these findings.</p><p><strong>Conclusion: </strong>Hypertension increases PhenoAge and is correlated with PhenoAge acceleration. The potential causal association between hypertension and multiple biological indicators of aging provides clues to the relationship between hypertension and epigenetic aging.</p>","PeriodicalId":10333,"journal":{"name":"Clinical and Experimental Hypertension","volume":"47 1","pages":"2559743"},"PeriodicalIF":3.5,"publicationDate":"2025-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145074674","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}
引用次数: 0
Association between serum albumin to serum creatinine ratio and incident heart failure in patients with chronic kidney disease. 慢性肾病患者血清白蛋白与血清肌酐比值与心力衰竭的关系
IF 3.5 4区 医学
Clinical and Experimental Hypertension Pub Date : 2025-12-31 Epub Date: 2025-09-30 DOI: 10.1080/10641963.2025.2561908
Weiwei Zhang, Youyou Liang, Peishan Xue, Chunlan Ma, Jing Zeng, Yali Qu, Yuting Zeng, Yingying Huang, Linhui He, Yuanyuan Jiang
{"title":"Association between serum albumin to serum creatinine ratio and incident heart failure in patients with chronic kidney disease.","authors":"Weiwei Zhang, Youyou Liang, Peishan Xue, Chunlan Ma, Jing Zeng, Yali Qu, Yuting Zeng, Yingying Huang, Linhui He, Yuanyuan Jiang","doi":"10.1080/10641963.2025.2561908","DOIUrl":"https://doi.org/10.1080/10641963.2025.2561908","url":null,"abstract":"<p><p>This prospective cohort study investigated the association between the albumin to serum creatinine ratio (sACR) and heart failure (HF) incidence in 150 chronic kidney disease (CKD) patients. Over a median 23-month follow-up, 114 HF events occurred. Multivariate Cox regression revealed a higher HF risk in the lowest versus highest sACR tertile (adjusted HR=1.742, 95% CI=1.341-2.002, p=0.023). Lower sACR correlated with worsened cardiac structure/function. The predictive AUC for HF was 0.64 for sACR alone and improved to 0.79 when combined with clinical covariates. We conclude that low sACR is independently associated with increased HF incidence in CKD patients.</p>","PeriodicalId":10333,"journal":{"name":"Clinical and Experimental Hypertension","volume":"47 1","pages":"2561908"},"PeriodicalIF":3.5,"publicationDate":"2025-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145198479","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}
引用次数: 0
Genetic causal assessment between major depression and hypertension: A two-sample bidirectional Mendelian randomization study. 重度抑郁症和高血压之间的遗传因果评估:一项双样本双向孟德尔随机化研究。
IF 3.5 4区 医学
Clinical and Experimental Hypertension Pub Date : 2025-12-31 Epub Date: 2025-09-11 DOI: 10.1080/10641963.2025.2553507
Yani Su, Ming Zhang, Peng Xu, Pengfei Wen, Ke Xu, Jiale Xie, Xianjie Wan, Lin Liu, Zhi Yang, Mingyi Yang
{"title":"Genetic causal assessment between major depression and hypertension: A two-sample bidirectional Mendelian randomization study.","authors":"Yani Su, Ming Zhang, Peng Xu, Pengfei Wen, Ke Xu, Jiale Xie, Xianjie Wan, Lin Liu, Zhi Yang, Mingyi Yang","doi":"10.1080/10641963.2025.2553507","DOIUrl":"https://doi.org/10.1080/10641963.2025.2553507","url":null,"abstract":"<p><strong>Objective: </strong>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.</p><p><strong>Methods: </strong>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.</p><p><strong>Results: </strong>The findings revealed a significant positive genetic causal association between major depression and hypertension (<i>P</i> = 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 (<i>P</i> = 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.</p><p><strong>Conclusion: </strong>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.</p>","PeriodicalId":10333,"journal":{"name":"Clinical and Experimental Hypertension","volume":"47 1","pages":"2553507"},"PeriodicalIF":3.5,"publicationDate":"2025-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145032849","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}
引用次数: 0
The effect of comprehensive intervention on children with anxiety/depression and increased blood pressure. 综合干预对儿童焦虑/抑郁及血压升高的影响。
IF 3.5 4区 医学
Clinical and Experimental Hypertension Pub Date : 2025-12-31 Epub Date: 2025-09-25 DOI: 10.1080/10641963.2025.2560635
Luxi Chen, Xin Wang, Lanmali Luo, Yanlin Li, Yilin Wu, Guanci Lv, Xiaofei Wu, Lanling Chen, Lijing Chen, Xizhou An, Benjuan Ying, Yuan Ding, Xin Chen, Xiaohua Liang
{"title":"The effect of comprehensive intervention on children with anxiety/depression and increased blood pressure.","authors":"Luxi Chen, Xin Wang, Lanmali Luo, Yanlin Li, Yilin Wu, Guanci Lv, Xiaofei Wu, Lanling Chen, Lijing Chen, Xizhou An, Benjuan Ying, Yuan Ding, Xin Chen, Xiaohua Liang","doi":"10.1080/10641963.2025.2560635","DOIUrl":"https://doi.org/10.1080/10641963.2025.2560635","url":null,"abstract":"<p><strong>Background: </strong>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.</p><p><strong>Methods: </strong>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.</p><p><strong>Results: </strong>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 (<i>P </i>< 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 (<i>P </i><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 <i>p</i> ≤ 0.05). The intervention activities decreased the blood pressure and BMI of the children with statistically significant differences (<i>p</i> < 0.05).</p><p><strong>Conclusion: </strong>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.</p>","PeriodicalId":10333,"journal":{"name":"Clinical and Experimental Hypertension","volume":"47 1","pages":"2560635"},"PeriodicalIF":3.5,"publicationDate":"2025-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145136689","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}
引用次数: 0
miPEP31 inhibits the vascular smooth muscle cell proliferation via cooperation with transcription factor Trps1. miPEP31通过与转录因子Trps1协同抑制血管平滑肌细胞增殖。
IF 3.5 4区 医学
Clinical and Experimental Hypertension Pub Date : 2025-12-31 Epub Date: 2025-09-22 DOI: 10.1080/10641963.2025.2561235
Gonghao Jiang, Xiangxiao Li, Zilong Fang, Guangzheng Shi, Xinran Tong, Peili Zhang, Qun Li, Wendong Chen
{"title":"miPEP31 inhibits the vascular smooth muscle cell proliferation via cooperation with transcription factor Trps1.","authors":"Gonghao Jiang, Xiangxiao Li, Zilong Fang, Guangzheng Shi, Xinran Tong, Peili Zhang, Qun Li, Wendong Chen","doi":"10.1080/10641963.2025.2561235","DOIUrl":"https://doi.org/10.1080/10641963.2025.2561235","url":null,"abstract":"<p><p>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.</p>","PeriodicalId":10333,"journal":{"name":"Clinical and Experimental Hypertension","volume":"47 1","pages":"2561235"},"PeriodicalIF":3.5,"publicationDate":"2025-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145124351","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}
引用次数: 0
Investigating non-invasive hemodynamic indicators in hypertension patients with coronary atherosclerotic heart disease. 高血压合并冠状动脉粥样硬化性心脏病患者无创血流动力学指标的研究
IF 3.5 4区 医学
Clinical and Experimental Hypertension Pub Date : 2025-12-31 Epub Date: 2025-10-06 DOI: 10.1080/10641963.2025.2564296
Xiaofen Tian, Yuanlin Zou, Yuyang Zhou, Yan Zhang, Zhe Huang, Nan Ding, Yang Yu
{"title":"Investigating non-invasive hemodynamic indicators in hypertension patients with coronary atherosclerotic heart disease.","authors":"Xiaofen Tian, Yuanlin Zou, Yuyang Zhou, Yan Zhang, Zhe Huang, Nan Ding, Yang Yu","doi":"10.1080/10641963.2025.2564296","DOIUrl":"https://doi.org/10.1080/10641963.2025.2564296","url":null,"abstract":"<p><strong>Objective: </strong>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.</p><p><strong>Methods: </strong>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.</p><p><strong>Results: </strong>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<sup>-1</sup> m<sup>-2</sup>) (all <i>p </i>< 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 <i>p </i>< 0.001). Strong negative correlations were detected between the hemodynamic parameters and CAD status (CO: <i>r</i> = -0.672, <i>p </i>< 0.001; SV: <i>r</i> = -0.589, <i>p </i>< 0.001), and positive correlations were detected between dyslipidemia and CAD (LDL-C: <i>r</i> = 0.458, <i>p </i>< 0.001; HDL-C: <i>r</i> = -0.381, <i>p </i>< 0.001).</p><p><strong>Conclusion: </strong>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.</p>","PeriodicalId":10333,"journal":{"name":"Clinical and Experimental Hypertension","volume":"47 1","pages":"2564296"},"PeriodicalIF":3.5,"publicationDate":"2025-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145231558","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}
引用次数: 0
Association of different diet quality scores with cardiovascular disease mortality risk in hypertension treatment group. 高血压治疗组不同饮食质量评分与心血管疾病死亡风险的关系
IF 3.5 4区 医学
Clinical and Experimental Hypertension Pub Date : 2025-12-31 Epub Date: 2025-09-29 DOI: 10.1080/10641963.2025.2563779
Junfeng Zhou, Yingjie Su, Liudang He, Ning Ding, Zhao Zeng
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