Hypertension最新文献

{"title":"Life-Course Blood Pressure Trajectories and Focal Myocardial Fibrosis in Older Age in MyoFit46.","authors":"Constantin-Cristian Topriceanu, Matthew Webber, Hunain Shiwani, Fiona Chan, Emma Martin, Debbie Falconer, Jonathan Bennett, Matthew A Stanley, Pablo Gonzalez-Martin, Haytham Shah, Swapnanil De, Mansoon Tamang, Isabelle Whitmore, Andrew Wong, Iain Pierce, Rhodri H Davies, Pier D Lambiase, Nandan Anavekar, Nishi Chaturvedi, Peter Kellman, Rebecca Hardy, James C Moon, Alun D Hughes, Gabriella Captur","doi":"10.1161/HYPERTENSIONAHA.126.26702","DOIUrl":"https://doi.org/10.1161/HYPERTENSIONAHA.126.26702","url":null,"abstract":"<p><strong>Background: </strong>The impact of life-course blood pressure (BP) trajectories on later-life focal left ventricular (LV) fibrosis by late gadolinium enhancement (LGE) remains elusive.</p><p><strong>Methods: </strong>MyoFit46 prospectively recruited ≈500 participants from a 1946 birth cohort for a cardiovascular magnetic resonance scan at 77 years, assessing LV LGE calculated using the 3-SD method or 5-SD method. Systolic BP (SBP) and diastolic BP were recorded at 36, 43, 53, 63, 69, and 77 years. For each participant, annual rates of BP change (steepness) and area under the BP trajectory (cumulative burden) for each age interval were calculated using mixed-effects models. Associations between life-course BPs and LGE were tested using generalized linear models, adjusted for antihypertensives, demographics, lifestyle, and comorbidities. Time-to-event associations between LGE and incident major adverse cardiovascular event (hospitalizations for coronary artery disease, stroke, heart failure, and atrial/ventricular arrhythmias; n=29) were also evaluated.</p><p><strong>Results: </strong>Among 472 participants (54% male), each 10 mm Hg greater individual SBPs at 36 to 69 years were associated with 6% to 11% greater LV LGE calculated using the 3-SD method (all <i>P</i>≤0.033), whereas each 10 mm Hg sustained greater SBPs on any age interval from 36 to 69 associated with 16% to 24% greater LGE calculated using the 3-SD method at 77(all <i>P</i>≤0.005), independent of SBP at 77 years. Each 1 mm Hg/y steeper SBP rise during age intervals 36 to 43, 43 to 53, and 53 to 63 was associated with 6% to 12% greater LGE calculated using the 3-SD method at 77 years. LGE presence was associated with greater major adverse cardiovascular event rates (hazard ratio, 2.5 [95% CI, 1.2-5.2]).</p><p><strong>Conclusions: </strong>Higher life-course BPs, cumulative burden, and steeper increases were associated with greater older-age LV LGE, which was linked to incident major adverse cardiovascular events. BP trajectories, beyond single-point BP measurements, warrant further investigation as tools to guide BP management strategies.</p>","PeriodicalId":13042,"journal":{"name":"Hypertension","volume":" ","pages":""},"PeriodicalIF":9.8,"publicationDate":"2026-10-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149220052","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":"Feedback Control of Arterial Pressure Using Deep Brain Stimulation: Transfer Function Analysis and Simulation Study.","authors":"Fumiyasu Yamasaki, Masato Seike, Takayoshi Hirota, Takayuki Sato","doi":"10.1161/HYPERTENSIONAHA.126.27225","DOIUrl":"https://doi.org/10.1161/HYPERTENSIONAHA.126.27225","url":null,"abstract":"<p><strong>Background: </strong>Deep brain stimulation (DBS) is an established treatment for Parkinson disease. Emerging evidence suggests that DBS of the subthalamic nuclei may be a target for neuromodulation therapy for orthostatic hypotension due to efferent baroreflex failure. To develop a central algorithm for an artificial baroreflex system, we first estimated the dynamic responses of arterial pressure to DBS, and then determined the feedback correction factors for DBS.</p><p><strong>Methods: </strong>A total of 14 Parkinson disease patients treated with DBS participated in submaximal stimulation screening tests for 20 s to identify responders exhibiting a pressor reaction of ≥10 mm Hg in systolic arterial pressure. In the responders, we randomly performed stimulation while tonometrically measuring the systolic arterial pressure. The transfer function from stimulation-to-systolic arterial pressure was computed using a fast Fourier transform algorithm. Finally, the feedback correction factors were determined via numerical simulations.</p><p><strong>Results: </strong>The transfer function was identifiable in all 3 responders. The average stimulation-to-systolic arterial pressure transfer function exhibited low-pass characteristics, with a steady-state gain of 8.24 mm Hg/stimulation, corner frequency of 0.02 Hz, and pure delay of 2.5 s. Based on these results, the proportional and integral correction factors were set to 0.12 and 0.018, respectively, for the feedback control of the stimulation. Computer simulations revealed that the system could quickly and effectively attenuate a sudden drop in systolic arterial pressure induced by external disturbances, such as head-up tilt.</p><p><strong>Conclusions: </strong>An artificial baroreflex system with the feedback correction of stimulation of DBS may be a novel therapeutic approach for efferent baroreflex failure.</p>","PeriodicalId":13042,"journal":{"name":"Hypertension","volume":" ","pages":""},"PeriodicalIF":9.8,"publicationDate":"2026-10-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149220070","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":"sFlt-1 in Decidua, Placenta, and Maternal Serum in Preeclampsia Subtypes.","authors":"Johanne Johnsen Rakner, Anders Hagen Jarmund, Åse Turid Rossevatn Svoren, Gabriela Brettas Silva, Bjørg Steinkjer, Camilla Kristoffersen, Sanjita Ravishankar, Raymond W Redline, Liv Cecilie Vestrheim Thomsen, Line Bjørge, Lobke Marijn Gierman, Ann-Charlotte Iversen","doi":"10.1161/HYPERTENSIONAHA.125.26640","DOIUrl":"https://doi.org/10.1161/HYPERTENSIONAHA.125.26640","url":null,"abstract":"<p><strong>Background: </strong>Soluble FMS-like tyrosine kinase (sFlt-1) drives maternal symptoms in preeclampsia, serves as a predictive biomarker, and represents a promising therapeutic target. sFlt-1 is expressed in placental and decidual tissue, which together form the maternal-fetal interface. Whether placental and decidual expression of sFlt-1 regulates the maternal serum levels remains unknown. This study aimed to investigate sFlt-1 expression and co-regulation in decidua, placenta, and maternal serum, in normal pregnancies and preeclamptic pregnancies with and without fetal growth restriction.</p><p><strong>Methods: </strong>Pregnant women with normal (n=65) or preeclamptic pregnancies with (n=42) or without (n=22) fetal growth restriction were included before cesarean delivery. sFlt-1 expression was quantified in maternal serum and umbilical cord blood (BRAHMS KRYPTOR) and by immunohistochemistry with semi-automated image analysis in decidual and placental tissue.</p><p><strong>Results: </strong>Decidual and placental sFlt-1 expression was trophoblast-dependent and selectively upregulated in preeclampsia without and with fetal growth restriction, respectively, and maternal serum sFlt-1 was elevated in both preeclampsia subtypes (<i>P</i><0.001, all comparisons). sFlt-1 expression showed a positive correlation between decidua and placenta but did not correlate with maternal serum levels. Maternal serum sFlt-1 levels diverged: with high levels (>11 500 pg/mL) only in preeclamptic pregnancies (n=21) and low levels (<11 500 pg/mL) in all normal pregnancies (n=28) and 42% (n=15) of preeclamptic pregnancies.</p><p><strong>Conclusions: </strong>sFlt-1 expression correlates across the maternal-fetal interface but is not directly reflected in maternal serum. The relationship to preeclampsia subtypes is complex.</p>","PeriodicalId":13042,"journal":{"name":"Hypertension","volume":" ","pages":""},"PeriodicalIF":9.8,"publicationDate":"2026-10-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149220085","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":"Aldosterone-Producing Lesions Harboring <i>ATP1A1</i> and <i>ATP2B3</i> Mutations: An International Multicenter Study.","authors":"Peeradon Vibhatavata, Yueting Liu, Madson Q Almeida, Laurence Amar, Irina Bancos, Stephanie Baron, Frederike Butz, Debbie L Cohen, Silas A Culver, Fabio Luiz Fernandes-Rosa, Augusto G Guimaraes, Amir H Hamrahian, Jinbo Hu, Markus Kroiss, James M Luther, Matthias F Oettle, Ismail Osman, Benjamin Pariente, Troy H Puar, Juilee Rege, Fumitoshi Satoh, Ute Scholl, Michael Stowasser, Yuta Tezuka, Aaron M Udager, Anand Vaidya, Desmaré van Rooyen, Heather Wachtel, Tracy A Williams, Vin-Cent Wu, Chun-Yi Wu, Maria-Christina Zennaro, William F Young, William E Rainey, Adina F Turcu","doi":"10.1161/HYPERTENSIONAHA.126.27798","DOIUrl":"https://doi.org/10.1161/HYPERTENSIONAHA.126.27798","url":null,"abstract":"<p><strong>Background: </strong>Somatic aldosterone-driver mutations are identified in >90% of patients with primary aldosteronism undergoing adrenalectomy, and they display distinct demographic clustering. <i>ATP1A1</i> and <i>ATP2B3</i> mutations, encoding the Na⁺/K⁺ ATPase α1 subunit and the Ca²⁺ ATPase 3, respectively, are relatively rare and are often grouped as <i>ATPase</i> mutations. Differences in their clinical and biochemical phenotypes remain understudied.</p><p><strong>Methods: </strong>This international collaboration of 16 centers included patients with primary aldosteronism harboring pathogenic variants in <i>ATP1A1</i> and <i>ATP2B3</i>. Clinical data were collected from medical records. Where available, we compared histopathologic features and steroid profiles (from peripheral and adrenal vein samples) by liquid chromatography-tandem mass spectrometry.</p><p><strong>Results: </strong>We included 300 patients (mean age, 57±11 years; 85% men) with aldosterone-producing lesions harboring <i>ATP1A1</i> (204) and <i>ATP2B3</i> (96) mutations. Age and sex distributions were similar. <i>ATP2B3</i> mutations were associated with lower serum potassium, higher lateralization indices, and stronger contralateral suppression. Postoperative biochemical cure was achieved in 96% of patients with <i>ATP2B3</i> mutations versus 83% of those with <i>ATP1A1</i> mutations (<i>P</i>=0.02). Multiple CYP11B2-positive lesions were observed in 47% of <i>ATP1A1</i> versus 27% of <i>ATP2B3</i> cases (<i>P</i>=0.03). Baseline peripheral steroid profiling was available in 126 patients (84 with <i>ATP1A1</i> and 42 with <i>ATP2B3</i>) and showed higher aldosterone concentrations in the <i>ATP2B3</i> group (median [interquartile range], 31 ng/dL [20-43] versus 23 ng/dL [11-38]; <i>P</i>=0.03).</p><p><strong>Conclusions: </strong><i>ATP</i>ase mutations are most common in middle-aged men with lateralized primary aldosteronism. Compared with <i>ATP1A1</i>, <i>ATP2B3</i> mutations are associated with a more severe primary aldosteronism phenotype, stronger lateralization, and higher rates of single aldosterone-producing lesions and postoperative biochemical cure.</p>","PeriodicalId":13042,"journal":{"name":"Hypertension","volume":" ","pages":""},"PeriodicalIF":9.8,"publicationDate":"2026-10-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149181527","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":"Glycosylated Fibronectin Compared With sFlt-1/PlGF Ratio for Preeclampsia Assessment.","authors":"Nouran Elbarbary, Chao Wang, Ramesh Ganapathy, Bini Ajay, Nick Anim-Nyame, Marcus Green, Sarah Fisher, Baskaran Thilaganathan, Amarnath Bhide","doi":"10.1161/HYPERTENSIONAHA.126.27232","DOIUrl":"https://doi.org/10.1161/HYPERTENSIONAHA.126.27232","url":null,"abstract":"<p><strong>Background: </strong>The ratio of sFlt-1 (soluble fms-like tyrosine kinase 1) to PlGF (placental growth factor) is an established biomarker for preeclampsia diagnostic triage. GlyFn (glycosylated fibronectin) measured by point-of-care testing is an alternative rapid assessment from finger-stick blood samples. This study was designed to test the hypothesis that the sensitivity of GlyFn is noninferior to that of the sFlt-1/PlGF ratio in women with suspected preeclampsia.</p><p><strong>Methods: </strong>This prospective observational study evaluated the diagnostic accuracy of both tests for preeclampsia in high-risk participants presenting between 24⁺⁰ and 36⁺⁶ weeks of gestation at 5 hospitals from January 2024 to July 2025. Participants underwent simultaneous point-of-care GlyFn testing (Lumella) and laboratory sFlt-1/PlGF ratio measurements. The primary outcome was birth for preeclampsia within 28 days of testing. Thresholds were set at GlyFn ≥350 μg/mL and sFlt-1/PlGF ratio ≥38. The noninferiority margin was predefined at 5%.</p><p><strong>Results: </strong>Among 397 participants, 59 (14.9%) had an indicated birth for preeclampsia within 28 days. GlyFn showed a sensitivity of 86.44% (95% CI, 75.02%-93.96%) compared with sFlt-1/PlGF 84.75% (95% CI, 73.01%-92.78%). Although sensitivities were numerically similar (<i>P</i>=0.79), the CI around the difference was too wide to establish noninferiority at the 5% margin. Negative predictive values were 96.40% and 96.59%, respectively. However, GlyFn had a lower specificity (63.31% versus 75.44%, <i>P</i><0.01).</p><p><strong>Conclusions: </strong>Point-of-care GlyFn testing showed similar sensitivity and negative predictive value to the sFlt-1/PlGF ratio for predicting an indicated birth for preeclampsia within 28 days. The point-of-care nature of the GlyFn test may facilitate immediate clinical decision-making in diverse healthcare settings.</p><p><strong>Registration: </strong>URL: https://doi.org/10.1186/ISRCTN13430018; Unique identifier: ISRCTN13430018.</p>","PeriodicalId":13042,"journal":{"name":"Hypertension","volume":" ","pages":""},"PeriodicalIF":9.8,"publicationDate":"2026-10-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149181586","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":"Inhibition of ROCK2 via KD025/Belumosudil Alleviates Hypertensive End-Organ Damage","authors":"Daniel J. Fehrenbach,C. Duncan Smart,Jean W. Wassenaar,Sharia Yasmin,Xinlan L. Li,Marisa N. Sepulveda,Ariane Imulinde Sugi,Hiroaki Shimokawa,Amanda C. Doran,Il-man Kim,Meena S. Madhur","doi":"10.1161/hypertensionaha.125.26418","DOIUrl":"https://doi.org/10.1161/hypertensionaha.125.26418","url":null,"abstract":"BACKGROUND: Despite achieving target blood pressure, hypertensive individuals have an elevated risk of cardiovascular disease, likely due to unresolved inflammation. Thus, adjunctive immune-modulating therapies are needed to protect patients with hypertension from end-organ damage. We previously showed that T helper 17 cells, which produce the proinflammatory cytokine IL (interleukin)-17A, contribute to hypertensive tissue injury. ROCK2 (Rho-associated coiled-coil–containing protein kinase 2) is a molecular switch governing T helper cell differentiation by promoting T helper 17 polarization and inhibiting T regulatory cell polarization. The present study tests whether T-cell–specific deletion of Rock2 or the Food and Drug Administration–approved ROCK2-specific inhibitor KD025/belumosudil protects against hypertension-associated end-organ damage. METHODS: T-cell–specific Rock2 knockout mice ( Rock2 fl/fl CD4 Cre+ ) and Rock2 fl/fl littermate controls were subjected to a 21-day deoxycorticosterone acetate–salt model of hypertension. In parallel, KD025/belumosudil treatment (50 mg/kg per day) starting after day 10 in wild-type mice was used to test the therapeutic potential of targeting ROCK2. Blood pressure, cardiac fibrosis, renal injury, and infiltration of immune cells were assessed. RESULTS: T-cell–specific Rock2 deletion in mice attenuated the hypertensive response in the deoxycorticosterone acetate–salt model and protected from cardiac and aortic fibrosis. KD025/belumosudil treatment did not reduce blood pressure but did decrease proinflammatory T helper 17 polarization in vivo and increased the cardiac regulatory T cells/T helper 17 ratio. Despite no blood pressure change, KD025 reduced cardiac and aortic fibrosis, improved echocardiographic and invasive hemodynamic indices, and attenuated albuminuria and renal T-cell infiltration. CONCLUSIONS: ROCK2 inhibition may serve as an adjunct immune-modulating therapy to mitigate the end-organ damage that occurs in the heart, vasculature, and kidney in hypertension.","PeriodicalId":13042,"journal":{"name":"Hypertension","volume":"19 1","pages":""},"PeriodicalIF":8.3,"publicationDate":"2026-10-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149088006","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":"Hemodynamics and Renin Profiles of Renal Artery Variations in Hypertensive CKD.","authors":"Hongkun Ma, Kexin Jin, Xueqin Xu, Ri Ji, Qingbing Wang, Zijin Chen, Chongjian Wang, Zhiyu Wang, Pingyan Shen, Xiaoyi Ding, Zhiyuan Wu, Wen Zhang","doi":"10.1161/HYPERTENSIONAHA.126.27130","DOIUrl":"10.1161/HYPERTENSIONAHA.126.27130","url":null,"abstract":"<p><strong>Background: </strong>The functional implications of renal artery variations-including accessory renal artery (ARA) and early branching-in hypertensive chronic kidney disease remain poorly understood.</p><p><strong>Methods: </strong>This prospective cohort study enrolled 38 patients with hypertensive chronic kidney disease and unilateral solitary renal artery variation (24 ARA, 14 early branching) undergoing pressure wire-based hemodynamic evaluation and selective segmental renal vein renin sampling; 35 patients completed 2-year follow-up.</p><p><strong>Results: </strong>Mean pressure gradient was higher in variant artery than in ipsilateral main (1.10±3.39 versus -0.15±2.21 mm Hg, <i>P</i>=0.04) and contralateral renal artery (versus -0.10±1.56 mm Hg, <i>P</i>=0.04) in the overall cohort, a difference limited to the ARA subgroup. Plasma renin activity was elevated in ARA-supplied segments compared with the ipsilateral main trunk (1.77±1.86 versus 1.24±1.40 ng/(mL·h), <i>P</i>=0.004) and contralateral artery-supplied segments (versus 1.24±1.37, <i>P</i>=0.002), whereas no significant difference was observed in the early branching subgroup. After multivariable adjustment, variant artery systolic pressure gradient was positively associated with variant-supplied segmental (β=0.41, <i>P</i>=0.02) and peripheral (β=0.37, <i>P</i>=0.04) plasma renin activity, angiotensin II, and nighttime mean arterial pressure. Peripheral aldosterone was associated with lower estimated glomerular filtration rate and higher urinary protein. All adjusted associations represent exploratory signals given limited sample size. Over 2 years, an intragroup estimated glomerular filtration rate decline was observed within the ARA subgroup (-5.2 mL/[min·1.73 m²]; <i>P</i>=0.02) while the early branching subgroup remained stable (<i>P</i>=0.47); however, the group-by-time interaction was not significant (<i>P</i>=0.06), indicating these preliminary trends require larger validation cohorts.</p><p><strong>Conclusions: </strong>Renal artery variations may alter intrarenal hemodynamics, with functional impairment and segmental renin hypersecretion observed primarily in ARA. This suggests a potential role for functional evaluation.</p>","PeriodicalId":13042,"journal":{"name":"Hypertension","volume":" ","pages":"e27130"},"PeriodicalIF":9.8,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148808507","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":"Professor John Low Reid, OBE, DM, FRCP, FRSE, FMedSci.","authors":"Anna F Dominiczak, Christian Delles, George S Stergiou, Matthew Walters, Ian B Wilkinson, Anthony Heagerty","doi":"10.1161/HYPERTENSIONAHA.126.27702","DOIUrl":"10.1161/HYPERTENSIONAHA.126.27702","url":null,"abstract":"","PeriodicalId":13042,"journal":{"name":"Hypertension","volume":" ","pages":"e27702"},"PeriodicalIF":9.8,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148759307","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":"Roles of Sirtuin-1 in the Prevention of Intracranial Aneurysm Rupture in Mice.","authors":"Hiroki Sato, Taichi Ikedo, Yushiro Take, Tetsuro Kimura, Takeshi Miyamoto, Daisuke Kudo, Redi Rahmani, Taichi Ishiguro, Hiroki Uchikawa, Takuma Maeda, Hitomi Sato, James Purcell, Jordan Morgan, Kyle Polen, Hiroki Kurita, Jinglu Ai, Satoru Eguchi, Michael T Lawton, Tomoki Hashimoto","doi":"10.1161/HYPERTENSIONAHA.125.26029","DOIUrl":"10.1161/HYPERTENSIONAHA.125.26029","url":null,"abstract":"<p><strong>Background: </strong>SIRT1 (sirtuin-1) regulates various cellular and metabolic processes in the vasculature. SIRT1 is an NAD⁺-dependent deacetylase that deacetylates transcription factors that control vascular inflammation and remodeling. Given that pathways regulated by SIRT1 are implicated in the pathophysiology of intracranial aneurysms, we hypothesized that activation and overexpression of SIRT1 prevent aneurysm rupture by suppressing vascular inflammation.</p><p><strong>Methods: </strong>Intracranial aneurysms were induced in mice by systemic hypertension and a single intracisternal injection of elastase. We analyzed the expression of SIRT1 in human and mouse aneurysms. We investigated the role of SIRT1 in aneurysm rupture using genetic overexpression of SIRT1 and cell-specific deletion in the endothelial, vascular smooth muscle, and myeloid lineages. We administered a SIRT1 activator and a SIRT1 inhibitor to assess the rupture rate and mRNA expression in cerebral arteries.</p><p><strong>Results: </strong>SIRT1 expression was significantly lower in intracranial aneurysm tissues than in control cerebral arteries in mice, with a similar trend in human aneurysms. Global overexpression of SIRT1 significantly decreased the rupture rate. Endothelial SIRT1 deletion increased the rupture rate, with no effect observed in other cell types. Inhibition of SIRT1 increased the rupture rate, whereas SIRT1 activation reduced the rupture rate and suppressed mRNA expression of proinflammatory cytokines in cerebral arteries.</p><p><strong>Conclusions: </strong>Our findings support a protective role of SIRT1 against intracranial aneurysm rupture in mice, with endothelial SIRT1 playing an important role in aneurysm stabilization. Pharmacological SIRT1 activation reduced aneurysm rupture and was associated with reduced vascular inflammation, providing a preclinical rationale for further investigation of SIRT1-related pathways.</p>","PeriodicalId":13042,"journal":{"name":"Hypertension","volume":" ","pages":"e26029"},"PeriodicalIF":9.8,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13437038/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148663739","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":"Brief Commentary on Blood Pressure, Pulse Wave Velocity, and Body Composition in Children and Adolescents.","authors":"Mieczysław Litwin","doi":"10.1161/HYPERTENSIONAHA.126.27742","DOIUrl":"https://doi.org/10.1161/HYPERTENSIONAHA.126.27742","url":null,"abstract":"","PeriodicalId":13042,"journal":{"name":"Hypertension","volume":"83 10","pages":"e27742"},"PeriodicalIF":9.8,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148982584","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}