CLINICAL AND EXPERIMENTAL HYPERTENSION临床与实验高血压
CLINICAL AND EXPERIMENTAL HYPERTENSION(英文缩写 CLIN EXP HYPERTENS),ISSN 1064-1963,eISSN 1525-6006,中文译名:临床与实验高血压 是一本学术期刊。本页汇总该期刊的最新影响因子、分区信息以及最新收录于 PubMed 的文献,帮助您快速了解期刊全貌。
发文量统计区间：2025-11-01 至 2026-10-31，按本站收录文献的发表日期统计。
期刊介绍
历年影响因子趋势
| JCR 数据年份 | 影响因子 | JCR 分区 |
|---|---|---|
| 2021 | 2.088 | Q4 |
| 2022 | 12.300 | Q1 |
| 2023 | 1.500 | Q3 |
| 2024 | 3.500 | Q2 |
| 2025 | 6.800 | Q1 |
CLINICAL AND EXPERIMENTAL HYPERTENSION 最新收录文献
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1. Efficacy and mechanistic insights of dapagliflozin in hypertension management.
1. 达格列净在高血压管理中的疗效及机制见解PMID:日期:2026-10-02Hypertension remains one of the leading modifiable risk factors for cardiovascular disease and premature mortality worldwide. Blood pressure (BP) management is particularly challenging in patients with coexisting type 2 diabetes (T2D), chronic kidney disease (CKD), or heart failure (HF). Sodium-glucose cotransporter 2 (SGLT2) inhibitors have become an integral component of contemporary cardiorenal therapy and have consistently demonstrated additional BP-lowering effects across diverse clinical settings. This narrative review synthesizes the current clinical evidence regarding the antihypertensive effects of dapagliflozin and summarizes the biological mechanisms that may contribute to these effects, including osmotic diuresis and natriuresis, weight reduction, modulation of the sympathetic nervous system, enhanced uric acid excretion, and attenuation of oxidative stress, inflammation, and vascular dysfunction. Across clinical studies, reductions in systolic BP (SBP) generally exceed those in diastolic BP (DBP), although the physiological basis underlying this differential response remains incompletely understood. Dapagliflozin has demonstrated good tolerability and antihypertensive effects in clinical applications, its long-term use may be limited by the risk of genital infections. Collectively, the available evidence supports dapagliflozin as a cardiorenal therapeutic agent that may provide additional BP-lowering benefits in patients with hypertension and concomitant T2D, CKD, or HF, rather than as a substitute for conventional antihypertensive therapy. Future hypertension-focused clinical studies are warranted to further define its role in hypertension management.
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2. Electroacupuncture in hypertension-mediated organ damage: A hypothesis-generating framework of blood pressure-dependent and candidate blood pressure-independent mechanisms.
2. 电针在高血压介导的靶器官损害中的作用：血压依赖性和候选血压非依赖性机制的假说生成框架PMID:日期:2026-09-10Contemporary hypertension management increasingly emphasizes hypertension-mediated organ damage (HMOD) rather than blood pressure (BP) targets alone. Electroacupuncture (EA) has been studied mainly as a non-pharmacological antihypertensive intervention, but whether its reported organ-level effects reflect BP lowering or additional tissue-level mechanisms remains unclear. This narrative mechanistic review synthesized preclinical and clinical literature from PubMed, Web of Science, Scopus and CNKI to organize EA-related evidence within a dual-pathway framework distinguishing BP-dependent from candidate BP-independent mechanisms across the brain, heart, kidney and vasculature. Preclinical evidence, mainly from spontaneously hypertensive rats, suggests that EA attenuates central sympathetic outflow, modulates brainstem-hypothalamic autonomic circuits, downregulates systemic and tissue renin-angiotensin-aldosterone system signaling, and reduces oxidative stress and inflammation. Organ-level evidence is graded moderate, and is the most developed of the four domains, for cardiac remodeling, including left ventricular hypertrophy and myocardial fibrosis; it is low-to-moderate for conduit-artery vascular changes and low for renal and cerebral effects. Across available studies, BP reduction and favorable organ-level changes occur together. No study has used BP-matched controls to isolate a BP-independent component, and no human trial with validated organ-specific HMOD endpoints was identified. Current evidence supports a hypothesis-generating dual-pathway framework in which EA-related organ effects may arise through BP-dependent mechanisms and candidate BP-independent tissue-level pathways. However, BP-independent organ protection remains unproven and requires BP-matched preclinical designs and sham-controlled human trials using validated HMOD surrogate endpoints.
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4. Associations of antihypertensive medication class with liver fibrosis and mortality in US adults with MASLD.
4. 降压药物类别与美国MASLD成人肝纤维化及死亡率的关联PMID:日期:2026-09-07Metabolic dysfunction-associated steatotic liver disease (MASLD) frequently coexists with hypertension, yet comparative data on antihypertensive medication classes remain limited. We examined associations between antihypertensive medication class and liver fibrosis and mortality in US adults with MASLD. We conducted a prevalent-user analysis using National Health and Nutrition Examination Survey (NHANES) 1999-2018 data linked to mortality through 2019. Antihypertensive exposure was defined at baseline based on self-reported medication use, consistent with a prevalent-user design. Steatosis was defined by the US Fatty Liver Index (US-FLI). Fibrosis was assessed using FIB-4 and APRI within a model-based framework derived from vibration-controlled transient elastography. Analyses comparing antihypertensive classes were restricted to monotherapy users. Logistic regression and Cox models with inverse probability of treatment weighting and survey weights were applied. Among participants with MASLD receiving antihypertensive monotherapy ( = 458; 86 deaths), ACEIs and ARBs were associated with lower all-cause mortality compared with calcium channel blockers (CCBs, reference group; = 47; 15 deaths) (ACEIs: adjusted hazard ratio [aHR], 0.30; 95% CI, 0.11-0.82; ARBs: 0.25; 95% CI, 0.07-0.94). In cross-sectional analyses, antihypertensive medication use was associated with lower odds of liver fibrosis defined by FIB-4 and APRI within US-FLI-defined populations (MASLD: FIB-4 aOR 0.51 [0.29-0.91]; APRI aOR 0.49 [0.28-0.89]). Findings were broadly consistent across sensitivity analyses, including alternative model specifications and expanded covariate adjustment. Antihypertensive medication use, particularly ACEIs and ARBs, was associated with lower fibrosis prevalence and all-cause mortality in MASLD. These findings are hypothesis-generating and require confirmation in prospective studies.
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5. Extracellular vesicles from the rostral ventrolateral medulla microenvironment regulate stress-induced hypertension via TNF-α-mediated modulation of neuronal excitability.
5. 延髓头端腹外侧区微环境来源的细胞外囊泡通过TNF-α介导的神经元兴奋性调节调控应激性高血压PMID:日期:2026-09-03Stress-induced hypertension (SIH) is driven by sympathetic overactivity, with the rostral ventrolateral medulla (RVLM) serving as a key regulatory hub. Extracellular vesicles (EVs) mediate intercellular communication, but their role in RVLM-related SIH pathogenesis remains unclear. A rat SIH model was established via 15 days of unpredictable stress. The EV secretion inhibitor GW4869 was microinjected into the RVLM of SIH rats to observe alterations in blood pressure and neuronal excitability. RVLM-EVs were isolated using iodixanol density gradient centrifugation and used to treat primary RVLM neurons in vitro; neuronal excitability was evaluated by c-FOS immunofluorescence staining. Bead-based flow cytometry was performed to detect the protein components of RVLM-EVs, and the TNF- antagonist R7050 was administered for both in vitro and in vivo interventions to examine its regulatory effects on neuronal excitability and blood pressure. GW4869 reduced BP and neuronal excitability in SIH rats. SIH-RVLM-EVs, with larger particle size, were internalized by primary RVLM neurons, enhancing excitability and inducing hypertension in normotensive rats. TNF- was enriched in SIH-RVLM-EVs; R7050 abrogated these pro-hypertensive effects in vitro and in vivo. RVLM-derived EVs promote SIH by delivering TNF-, which enhances RVLM pre-sympathetic neuronal excitability and sympathetic overactivity. TNF- in RVLM-EVs is a promising therapeutic target for SIH.
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6. Adipose-derived microRNA-518a drives hepatic cholesterol dysregulation and hypertension-related vascular remodeling in metabolic dysfunction-associated steatohepatitis via the MST1-AMPK-SREBP2 axis.
6. 脂肪来源的microRNA-518a通过MST1-AMPK-SREBP2轴驱动代谢功能障碍相关脂肪性肝炎中的肝脏胆固醇失调和高血压相关血管重塑PMID:日期:2026-09-02Metabolic dysfunction-associated steatohepatitis (MASH) is characterized by disrupted hepatic lipid homeostasis and progressive liver injury, and frequently coexists with hypertension and systemic vascular remodeling, suggesting shared pathophysiological mechanisms. Although adipose tissue-derived microRNAs have emerged as important mediators of inter-organ communication, their roles in regulating hepatic cholesterol metabolism and vascular dysfunction during MASH remain incompletely understood. This study aimed to investigate whether microRNA-518a regulates hepatic cholesterol metabolism and MASH progression through the MST1-AMPK-SREBP2 signaling pathway and to explore its potential implications for vascular remodeling and hypertension. Integrative bioinformatic analyses, including Mendelian randomization and transcriptomic network analysis, were performed to identify candidate regulatory pathways associated with MASH. Functional validation was conducted using human clinical samples, in vitro cell models, exosome-mediated microRNA delivery, and a dietary mouse model of MASH. MST1 was identified as a key regulatory target of microRNA-518a. Increased microRNA-518a expression suppressed MST1, resulting in reduced AMPK activation and enhanced SREBP2-mediated cholesterol biosynthesis. Functional experiments demonstrated that microRNA-518a promoted hepatic cholesterol accumulation, lipid deposition, inflammation, and fibrotic changes, whereas restoration of MST1 partially reversed these effects. Exosome-mediated delivery of microRNA-518a further supported its ability to modulate hepatic metabolic responses through intercellular communication. MicroRNA-518a promotes hepatic cholesterol dysregulation and MASH progression by targeting the MST1-AMPK-SREBP2 signaling pathway. Notably, the convergence of this axis with vascular regulatory networks suggests broader implications for understanding the metabolic-vascular comorbidities frequently observed in MASH patients, including hypertension and arterial stiffness.
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7. Integrated multi-omics analyses identify an RAS-SLC11A2-associated molecular framework linking iron metabolism with PCOS-related cardiometabolic risk.
7. 整合多组学分析识别出一个与RAS-SLC11A2相关的分子框架，将铁代谢与多囊卵巢综合征相关的心血管代谢风险联系起来PMID:日期:2026-09-01PCOS is a common endocrine disorder with elevated cardiometabolic risk, yet the role of the renin-angiotensin system (RAS)-iron metabolism axis in this comorbidity remains unclear. We explored its underlying mechanisms and evaluated the therapeutic potential of gentiopicroside. Integrated multi-omics analyses combining transcriptomics, single-cell RNA sequencing, Mendelian randomization, machine learning, molecular docking, and functional assays were performed to identify shared molecular pathways and therapeutic targets across PCOS, hypertension, NAFLD, and T2DM. SLC11A2 was consistently dysregulated in PCOS transcriptomic datasets, and associated with iron metabolism, inflammatory response and oxidative stress pathways. Genetic analyses validated RAS-related regulation in hypertension susceptibility and revealed shared genetic architecture between PCOS and cardiometabolic traits. Network and single-cell analyses characterized SLC11A2-associated molecular patterns in disease-relevant cell types; machine learning identified disease-classifying molecular signatures. Gentiopicroside alleviated inflammatory and oxidative stress phenotypes, including reduced IL-6 expression and reactive oxygen species accumulation. This study defines an RAS-SLC11A2 molecular framework linking iron metabolism dysregulation to PCOS-related cardiometabolic risk, elucidating the mechanisms connecting ovarian dysfunction, inflammation, oxidative stress and hypertension, and supports gentiopicroside as a promising therapeutic candidate.
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9. Inter-ankle systolic blood pressure difference is associated with microalbuminuria in non-diabetic hypertension patients: A cross-sectional study from two cohorts.
9. 踝间收缩压差与非糖尿病高血压患者的微量白蛋白尿相关：一项来自两个队列的横断面研究PMID:日期:2026-08-03[中文摘要] 这项横断面研究旨在分析踝间收缩压差值（sIAND）是否与高血压肾损害的不同阶段相关。研究从两个队列中纳入了1，658例和831例非糖尿病高血压患者。高血压肾损害通过尿白蛋白与肌酐比值（UACR）、胱抑素C和估算肾小球滤过率来反映。Logistic回归结果显示，sIAND仅独立地与以微量白蛋白尿（UACR > 30 mg/g）反映的亚临床高血压肾损害相关。受试者工作特征曲线表明，sIAND能更有效地识别微量白蛋白尿。sIAND有助于识别微量白蛋白尿，为风险分层和临床管理提供有用的线索。
[英文摘要] This cross-sectional study aimed to analyze whether inter-ankle systolic blood pressure difference (sIAND) was associated with different stages of hypertensive renal damage. 1,658 and 831 nondiabetic hypertensive patients were included from two cohorts. The hypertensive renal damage was reflected by urinary albumin-to-creatinine ratio (UACR), Cystatin C, and estimated glomerular filtration rate. Logistic regression results showed that sIAND was only associated with subclinical hypertensive renal damage reflected by microalbuminuria (UACR > 30 mg/g) independently. Receiver operating characteristic curves indicated sIAND can identify microalbuminuria more effectively. sIAND can aid in identifying microalbuminuria to provide useful clues for risk stratification and clinical management.
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10. Early prediction of preeclampsia among the advanced-age pregnant women: A retrospective multicenter study.
10. 高龄孕妇先兆子痫的早期预测：一项回顾性多中心研究PMID:日期:2026-08-03Preeclampsia (PE) remains a leading cause of maternal and perinatal morbidity. Women of advanced maternal age (AMA, ≥ 35 years) constitute a rapidly expanding high-risk subpopulation in China. Existing first-trimester prediction models were derived in general obstetric populations and often rely on specialized biophysical or proprietary biomarker assays, with limited validation in AMA women. This multicenter retrospective study enrolled 2,582 AMA pregnant women from three tertiary centers in southern China, partitioned into a training cohort ( = 1,327), an internal validation cohort ( = 569), and two external validation cohorts ( = 399 and 287). Predictors were selected using LASSO and multivariable logistic regression and assembled into a nomogram. Performance was evaluated by area under the receiver operating characteristic curve (AUC), calibration, Brier scores, decision curve analysis, and clinical impact curves. Seven independent predictors were retained: pre-pregnancy BMI, parity, mode of conception, uric acid, white blood cell count, red blood cell count, and hemoglobin. The nomogram achieved AUCs of 0.819, 0.795, 0.787, and 0.756 across the four cohorts, with close calibration and favorable net benefit. Performance was preserved when women with chronic hypertension were included and across early-onset and late-onset PE subgroups. Notably, maternal age itself was not discriminative within the AMA stratum ( = 0.626). This nomogram relying exclusively on routine clinical and laboratory parameters provides an accessible tool for individualized early-pregnancy PE risk assessment and risk-stratified antenatal management in AMA women.