Hypertension最新文献

{"title":"Correction to: Role of the Renin-Angiotensin System in Blood Pressure Regulation in Smooth Muscle-Specific Cullin-3 Deficient Mice.","authors":"Daria Golosova, Gaurav Kumar, Nisita Chaihongsa, John J Reho, Ko-Ting Lu, Daniel T Brozoski, Kelsey K Wackman, Samuel B R Lawton, Patricia C Muskus, Brian L Lin, Justin L Grobe, Pablo Nakagawa, Curt D Sigmund","doi":"10.1161/HYP.0000000000000255","DOIUrl":"https://doi.org/10.1161/HYP.0000000000000255","url":null,"abstract":"","PeriodicalId":13042,"journal":{"name":"Hypertension","volume":"82 11","pages":"e348"},"PeriodicalIF":8.2,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145299980","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Advancing Risk-Based Approaches in Blood Pressure Management: Reflections on the 2025 AHA/ACC Statement.","authors":"Kazem Rahimi, Milad Nazarzadeh, Anthony Rodgers","doi":"10.1161/HYPERTENSIONAHA.125.25564","DOIUrl":"10.1161/HYPERTENSIONAHA.125.25564","url":null,"abstract":"","PeriodicalId":13042,"journal":{"name":"Hypertension","volume":" ","pages":"1794-1798"},"PeriodicalIF":8.2,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12529973/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144952159","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cardiovascular Effects of Sucrose in Experimental Animals and Humans.","authors":"Yuki Nakayama, Katherine J Elliott, Satoru Eguchi","doi":"10.1161/HYPERTENSIONAHA.125.25720","DOIUrl":"10.1161/HYPERTENSIONAHA.125.25720","url":null,"abstract":"<p><p>Sucrose, a disaccharide composed of glucose and fructose, is one of the most widely consumed dietary sugars. The recent global rise in sugar intake is a growing concern regarding its potential contribution to the development of metabolic and cardiovascular disorders. While the metabolic effects of glucose and fructose have been extensively studied individually, the impact of sucrose on cardiovascular health remains an evolving area of research. In rats with a high-sucrose diet, hallmarks of metabolic syndrome were observed including weight gain, insulin resistance, ≈15-mm Hg elevation in blood pressure, and systemic inflammation. It also caused disruptions in gut microbiota. Recently, we reported that high-sucrose ingestion via drinking water induces hypertension and cardiovascular complications associated with hyperinsulinemia in mice. In humans, excessive sucrose intake is associated with elevated plasma glucose, insulin, and lipid levels, particularly in individuals with obesity. Although long-term epidemiological data are limited, a recent study demonstrated that sucrose intake increased the risk for hypertension in women. These findings highlight the need to reassess the relationship between sucrose consumption and cardiovascular disease in humans. This review discusses current evidence from both animal and human studies covering molecular mechanisms and pathophysiological outcomes to explore how sucrose influences cardiovascular and metabolic health. As sucrose remains a major component of global diets, particularly in industrialized nations, further longitudinal and mechanistic studies are needed to clarify its long-term health consequences. Reducing excess sucrose intake may represent a prudent public health strategy, especially for individuals at increased risk for cardiovascular diseases including hypertension.</p>","PeriodicalId":13042,"journal":{"name":"Hypertension","volume":" ","pages":"1799-1808"},"PeriodicalIF":8.2,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12535405/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144952141","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"ITLN1 Improves Endothelial Dysfunction in Hypertensive Mice via Wnt5b-JNK Signaling.","authors":"Aiqin Mao, Zicheng Li, Xiaoming Shi, Ka Zhang, Hao Kan, Li Geng, Jing Shao, Dongxu He","doi":"10.1161/HYPERTENSIONAHA.125.25275","DOIUrl":"https://doi.org/10.1161/HYPERTENSIONAHA.125.25275","url":null,"abstract":"<p><strong>Background: </strong>Hypertension is a prevalent cardiovascular disorder involving endothelial cell dysfunction. ITLN1 (Intelectin-1) is a fat-derived secreted adipokine that has been shown to enhance endothelium-dependent vasodilation through molecular signaling pathways that remain unclear.</p><p><strong>Methods: </strong>First, we generated endothelial-specific ITLN1 knockout (ITLN1_EC^-/-) mice to evaluate the functional consequences of ITLN1 deficiency on vascular homeostasis. Subsequently, experiments combining RNA sequencing, quantitative real-time PCR, immunoblotting, immunofluorescence, and nitric oxide quantification were used to elucidate the underlying signaling pathways involved. Finally, virtual molecular docking was used to identify puerarin 6-O-xyloside as a selective ITLN1-binding compound.</p><p><strong>Results: </strong>Hypertensive mice presented reduced ITLN1 abundance and decreased endothelial ITLN1 mRNA levels. Further studies revealed that ITLN1 overexpression via adenoviral vectors improved vascular relaxation in hypertensive models. Mechanistically, ITLN1 restored endothelial nitric oxide synthase phosphorylation by suppressing Wnt5b-JNK (c-jun N-terminal kinase) signaling, thereby increasing nitric oxide production. We subsequently elucidated ITLN1-modulating molecules and found that puerarin 6-O-xyloside upregulated ITLN1 expression and augmented vasodilation. Finally, ZNF460 was identified as a transcriptional repressor of ITLN1 in endothelial cells.</p><p><strong>Conclusions: </strong>This study identified ITLN1 as a potential therapeutic target for hypertension. Upregulating ITLN1 protected against endothelial dysfunction by modulating Wnt5b-JNK/endothelial nitric oxide synthase signaling, with puerarin 6-O-xyloside serving as a promising ITLN1 activator.</p>","PeriodicalId":13042,"journal":{"name":"Hypertension","volume":"82 11","pages":"1987-1998"},"PeriodicalIF":8.2,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145300041","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Subclinical Postpartum Renal Structure After Hypertensive Pregnancy Disorders.","authors":"Hannah R Cutler, Jamie Kitt, Prenali D Sattwika, Lucy E M Finnigan, Ana Estevez-Fernandez, Yvonne Kenworthy, Katie Suriano, Annabelle Frost, Samuel Krasner, Casey Johnson, Annabelle McCourt, Rebecca Mills, Katherine Tucker, Alexandra Cairns, Cristian Roman, Christina Aye, Lucy Mackillop, Basky Thilaganathan, Lucy C Chappell, Betty Raman, Adam J Lewandowski, Winok Lapidaire, Paul Leeson","doi":"10.1161/HYPERTENSIONAHA.125.25130","DOIUrl":"10.1161/HYPERTENSIONAHA.125.25130","url":null,"abstract":"<p><strong>Background: </strong>Hypertensive pregnancies are associated with increased risks of renal failure in pregnancy and later life. However, traditional markers of renal function normalize postpartum, making identification of those at future disease risk difficult. We studied whether the type and severity of hypertensive pregnancy associated with postpartum renal structure.</p><p><strong>Methods: </strong>One hundred and twenty-five women from interventional trials (61 preeclamptic, 33 gestational hypertension, and 31 normotensive pregnancy), aged ≥18 years, were imaged using magnetic resonance imaging 6 to 12 months postpartum. Anthropometric, demographic, blood pressure, and blood sample data were collected during pregnancy and postpartum. Kidney volume indexed to body surface area and corticomedullary differentiation were compared between groups using a 1-way ANCOVA, whereas associations with other outcomes were assessed using correlation tests.</p><p><strong>Results: </strong>Postpartum total kidney volume indexed to body surface area was smaller in women who had preeclampsia compared with those who had gestational hypertension or a normotensive pregnancy (<i>P</i>=0.049). Total kidney volume postpartum correlated with estimated glomerular filtration rate at delivery (<i>P</i><0.001). However, smaller volumes were not explained by reduced corticomedullary differentiation, which only differed in women with gestational hypertension compared with preeclamptic (<i>P</i>=0.02) and normotensive women (<i>P</i>=0.007). There were no associations between renal measures and blood pressure during or after pregnancy.</p><p><strong>Conclusions: </strong>At 6 to 12 months postpartum, preeclamptic women have smaller kidney volumes than women with gestational hypertension or normotensive pregnancies. These smaller volumes relate to lower renal function at delivery but not corticomedullary differentiation, which only differed in women with gestational hypertension.</p><p><strong>Registration: </strong>URL: https://www.clinicaltrials.gov; Unique identifiers: NCT04273854 and NCT05434195.</p>","PeriodicalId":13042,"journal":{"name":"Hypertension","volume":" ","pages":"1948-1958"},"PeriodicalIF":8.2,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12529983/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144952121","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Sex Hormone Androgen Elevates Blood Pressure Through Gut Microbiota-TMAO Pathway.","authors":"Ying Li, Hong-Li Jiang, Lei Chen, Jia-Yue Yu, Sachin Aryal, Ya-Nan Gao, Ying-Bao Zhu, Wen-Fang Lu, Zhi-Ming Dai, Li-Li Huang, Qi Liu, Hua Liu, Li-Min Wei, Xue Zhao, Xiao-Min Liu, Juan Bai, Xiao-Lian Shi, Qing Su, Meng-Lu Xu, Ishan Manandhar, Pritam Bardhan, Ya-Nan Wang, Ting Yao, Bina Joe, Tao Yang, Hong-Bao Li","doi":"10.1161/HYPERTENSIONAHA.125.25052","DOIUrl":"10.1161/HYPERTENSIONAHA.125.25052","url":null,"abstract":"<p><strong>Background: </strong>Hypertension is a leading risk factor for all-cause mortality worldwide, affecting ≈1.3 billion people. Imbalanced gut microbiota contributes to blood pressure elevation. We recently reported sex differences in the responses of gut microbiota to environmental stimuli, such as salt, with male gut microbiota being more vulnerable to induce high blood pressure than female microbiota. In this study, we investigated the mechanisms by which gut microbiota regulate blood pressure in a sex-dependent manner.</p><p><strong>Methods: </strong>Antibiotic treatment, gonadectomy, sex hormone replenishment, and treatment with trimethylamine N-oxide or its blocker were performed in male and female spontaneously hypertensive rats.</p><p><strong>Results: </strong>We observed sex differences in gut microbiota composition and sex-specific blood pressure responses to antibiotic treatment in pubertal spontaneously hypertensive rats. In gonadectomized rats treated with sex hormones, we found that the male sex hormone dihydrotestosterone elevated blood pressure, reshaped gut microbiota, and increased levels of microbiota-derived metabolites, trimethylamine and trimethylamine N-oxide. The accumulation of trimethylamine N-oxide in plasma and the paraventricular nucleus of the hypothalamus was associated with inflammation and sympathetic activation.</p><p><strong>Conclusions: </strong>These findings underscore the mechanistic role of dihydrotestosterone in gut microbiota-mediated sex-specific blood pressure regulation and suggest that targeting the gut microbiota-treatment with trimethylamine N-oxide pathway may provide new therapeutic strategies for male hypertension.</p>","PeriodicalId":13042,"journal":{"name":"Hypertension","volume":" ","pages":"1999-2011"},"PeriodicalIF":8.2,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144882804","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"c-Fos Mediates Preeclampsia Through p-AMPK/Detyrosinated Tubulin Pathway.","authors":"Yihong Huang, Shanshan Zhao, Chumei Zeng, Shaole Shi, Zhuyu Li, Lixia Shen, Huizhen Geng, Zilian Wang, Dongyu Wang","doi":"10.1161/HYPERTENSIONAHA.124.24416","DOIUrl":"10.1161/HYPERTENSIONAHA.124.24416","url":null,"abstract":"<p><strong>Background: </strong>Preeclampsia is a systemic disorder unique to pregnancy that is associated with trophoblast dysfunction. Although the c-Fos (Fos proto-oncogene) is essential for placental development, its mechanistic role in preeclampsia remains unclear.</p><p><strong>Methods: </strong>We identified c-Fos as a hub gene through an analysis of cell-free RNA from maternal plasma and single-cell RNA sequencing of preeclamptic placentas. We assessed c-Fos expression in the placenta and plasma and examined its correlation with lipids. Functional changes upon the viral modulation of c-Fos in trophoblast cells were evaluated. Untargeted lipidomics and RNA sequencing were conducted to uncover the downstream mechanisms, and the findings were validated in trophoblast cells and a preeclampsia-like murine model.</p><p><strong>Results: </strong>c-Fos expression was decreased in maternal peripheral plasma from early to mid-pregnancy and in the placenta of preeclampsia patients. Furthermore, c-Fos expression levels were negatively correlated with neutral lipid accumulation. c-Fos deficiency impaired trophoblast invasion, proliferation, and syncytialization while promoting apoptosis. Reduced c-Fos expression also led to lipid droplet aggregation and mitochondrial dysfunction. Mechanistically, c-Fos silencing inhibited the p-AMPK (phosphorylated AMP-activated protein kinase)/detyrosinated tubulin pathway, disrupting lipid droplet trafficking and metabolism and promoting lipid droplet accumulation and an altered lipid profile. c-Fos deficiency induced a preeclampsia-like phenotype in mice, whereas c-Fos overexpression partially alleviated preeclampsia symptoms.</p><p><strong>Conclusions: </strong>c-Fos downregulation inhibits the p-AMPK/detyrosinated tubulin pathway, driving lipid droplet accumulation and consequent trophoblast dysfunction, revealing c-Fos as a potential therapeutic target for preeclampsia.</p>","PeriodicalId":13042,"journal":{"name":"Hypertension","volume":" ","pages":"1959-1974"},"PeriodicalIF":8.2,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144952085","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Relationship Between Home Blood Pressure Monitoring-Confirmed Resistant Hypertension and Cardiovascular Prognosis.","authors":"Kazuomi Kario,Yukie Okawara,Hiroshi Kanegae,Naoko Tomitani,Satoshi Hoshide","doi":"10.1161/hypertensionaha.125.25747","DOIUrl":"https://doi.org/10.1161/hypertensionaha.125.25747","url":null,"abstract":"BACKGROUNDCardiovascular prognosis in people with drug-resistant hypertension, defined by office and home blood pressure, has not been fully evaluated. This Japan Morning Surge-Home Blood Pressure study data analysis evaluated the cardiovascular event rate in patients with drug-resistant hypertension defined using office and home blood pressure.METHODSThe incidence of cardiovascular events (stroke, coronary artery disease, congestive heart failure, aortic dissection) in participants with true resistant hypertension (office blood pressure ≥140/90 mm Hg and home blood pressure ≥135/85 mm Hg during treatment with ≥3 antihypertensives, including a diuretic) was determined and compared with other hypertension subgroups.RESULTSDuring mean 6.2 years' follow-up in 4278 participants (mean age, 64.9±10.9 years; 46.9% male), cardiovascular events included stroke (n=96), coronary artery disease (n=125), congestive heart failure (n=42), aortic dissection (n=8), and sudden death (n=15). The incidence of cardiovascular events in patients with home blood pressure monitoring-confirmed resistant hypertension was 34.7 per 1000 person-years (significantly higher than in those with well-controlled hypertension on ≥3 drugs including a diuretic; 11.9 per 1000 person-years [P<0.001]). In the home blood pressure monitoring-confirmed resistant hypertension group, cardiovascular event incidence was highest in those with versus without cardiovascular disease history (39.4 versus 22.7 per 1000 person-years).CONCLUSIONSThese data showed that home blood pressure-confirmed resistant hypertension was associated with a high incidence of cardiovascular events over time, especially in the presence of a cardiovascular disease history. The relevance of home blood pressure monitoring for defining resistant hypertension and treatment strategies, especially compared with ambulatory blood pressure monitoring, remains to be determined.REGISTRATIONURL: https://www.umin.ac.jp/ctr; Unique identifier: UMIN000000894.","PeriodicalId":13042,"journal":{"name":"Hypertension","volume":"3 1","pages":""},"PeriodicalIF":8.3,"publicationDate":"2025-10-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145339014","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effect of Nocturia and Sleep Quality on Sleep Blood Pressure: The HI-JAMP Study.","authors":"Naoko Tomitani,Satoshi Hoshide,Kazuomi Kario","doi":"10.1161/hypertensionaha.125.25497","DOIUrl":"https://doi.org/10.1161/hypertensionaha.125.25497","url":null,"abstract":"BACKGROUNDBlood pressure (BP) during sleep is known to be affected by sleep disturbance, including nocturia and sleep disorders. This study investigated the effect of nocturia and self-reported poor sleep on BP using a multisensor BP monitoring device (TM-2441; A&D Co) equipped with an accelerator.METHODSThis analysis is part of the HI-JAMP study (Home-Activity ICT-based Japan Ambulatory Blood Pressure Monitoring Prospective), in which 24-hour ambulatory BP monitoring with simultaneously monitored physical activity using a multisensor all-in-one device was performed in hypertensive patients taking at least 1 antihypertensive agent. Sleep time, awake time, nocturia frequency, and sleep assessment on the ambulatory BP monitoring night were collected from a self-report diary. Nighttime BP was defined as the BP measured between self-reported sleep and awakening times. Sleep BP was defined as the BP without physical activity during a sleep period.RESULTSData of 1252 individuals (mean age, 67.4±11.7 years; mean body mass index, 24.8±3.9 kg/m2; 58.2% male) were analyzed. Averages of sleep systolic BP (SBP) were lower than those of nighttime SBP (113.9±15.8 versus 115.2±15.5 mm Hg; P<0.001). Frequency of nocturnal voids was associated with an increase in nighttime systolic SBP (1-2×: 4.7 mm Hg, P<0.001; ≥3×: 9.6 mm Hg, P<0.001) and sleep SBP (1-2×: 4.1 mm Hg, P<0.001; ≥3×: 8.5 mm Hg, P<0.001). Self-reported poor sleep showed a marginal association with increased nighttime SBP but was not associated with sleep SBP.CONCLUSIONSCompared with self-reported poor sleep, nocturia had a greater impact on BP during sleep, even after excluding BP readings with nocturnal physical activity.REGISTRATIONUnique identifier: UMIN000029151.","PeriodicalId":13042,"journal":{"name":"Hypertension","volume":"102 1","pages":""},"PeriodicalIF":8.3,"publicationDate":"2025-10-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145339323","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effects of Dietary Sodium Modulation on Circulating Extracellular Vesicles.","authors":"Jacopo Burrello,Fabrizio Buffolo,Brooke Honzel,Laura Tsai,Martina Tetti,Alessio Burrello,Dario Di Silvestre,Pierluigi Mauri,Virginia Capuzzo,Stefania Bruno,Lucio Barile,Paolo Mulatero,Anand Vaidya,Silvia Monticone","doi":"10.1161/hypertensionaha.125.25101","DOIUrl":"https://doi.org/10.1161/hypertensionaha.125.25101","url":null,"abstract":"BACKGROUNDSodium is involved in osmoregulation, fluid balance, and immune system function. High sodium (HS) consumption is linked to endothelial dysfunction, hypertension, and mortality. Extracellular vesicles (EVs), nano-sized particles reflecting cellular status, could link dietary sodium to vascular and immune changes. This study aimed to characterize circulating EVs and assess their functional role on endothelial cells after dietary sodium modulation.METHODSFifty subjects underwent 2 dietary sodium interventions, each lasting 5 to 7 days: sodium-restriction (10-40 mmol/d, 0.23-0.92 g/d) followed by sodium-loading (intake above 180 mmol/d, 4.14 g/d). Serum EVs were isolated after each phase and analyzed using a flow cytometry bead-based platform. Bioinformatics identified intracellular targets of EV surface antigens upregulated after the HS diet. Human microvascular endothelial cells were used to assess EV effects in vitro.RESULTSIn matched comparison, after HS-diet, EVs exhibited increased levels of CD14-CD25-CD40 (immune system markers), CD29-CD42-CD62P (coagulation and platelets activation markers), and CD31 (endothelial marker). Among targets identified by signaling network analysis, the incubation of human microvascular endothelial cells with patient-derived EVs after HS-diet resulted in decreased expression of AKT1, increased expression of MAPK3, and levels of active RhoA. It also resulted in increased expression of ICAM1, the number of ICAM-1 positive human microvascular endothelial cells, and nitric oxide levels.CONCLUSIONSDietary sodium modulates the expression of EV surface antigens associated with vascular inflammation, platelet activation, and endothelial function. Circulating EVs may mediate the effects of HS condition by interacting with endothelial cells, through multiple pathways, including RhoA activation and increased ICAM-1 expression.","PeriodicalId":13042,"journal":{"name":"Hypertension","volume":"26 1","pages":""},"PeriodicalIF":8.3,"publicationDate":"2025-10-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145339324","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}