Hypertension最新文献

{"title":"In Memoriam: Allyn L. Mark.","authors":"Gerald F DiBona, Donald D Heistad","doi":"10.1161/HYPERTENSIONAHA.125.25103","DOIUrl":"https://doi.org/10.1161/HYPERTENSIONAHA.125.25103","url":null,"abstract":"","PeriodicalId":13042,"journal":{"name":"Hypertension","volume":"82 7","pages":"e108-e109"},"PeriodicalIF":6.9,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144325521","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":"ca-circSCN8A Promotes HPASMCs Ferroptosis via LLPS Initiated R-Loop.","authors":"Mengnan Li, Yingying Hao, Xinyue Song, Huiyu Liu, Chi Zhang, Jiaqi Zhang, Hanliang Sun, Xiaodong Zheng, Lixin Zhang, Hang Yu, Cui Ma, Xijuan Zhao, Daling Zhu","doi":"10.1161/HYPERTENSIONAHA.125.25036","DOIUrl":"10.1161/HYPERTENSIONAHA.125.25036","url":null,"abstract":"<p><strong>Background: </strong>Ferroptosis has been implicated in pulmonary hypertension (PH), and chromatin-associated RNAs are increasingly recognized as key regulators of this process. However, the detailed mechanism remains unexplored.</p><p><strong>Methods: </strong>Bioinformatics, Sanger sequencing, and RNase R digestion were used to identify the upregulation of ca-circSCN8A. Functional gain and loss assays were used to unveil the role of ca-circSCN8A in hypoxic redox-dependent ferroptosis in human pulmonary arterial smooth muscle cells and a PH mice model. Interaction between ca-circSCN8A and FUS was detected via RNA immunoprecipitation and pull-down assays. Fluorescence recovery after photobleaching, ChIRP-qPCR (Chromatin Isolation by RNA Purification followed by Quatitative PCR), malondialdehyde, reduced glutathione, and glutathione were conducted to explore the potential molecular mechanism.</p><p><strong>Results: </strong>ca-circSCN8A was identified and confirmed to be upregulated in PH. Its overexpression promoted hypoxia-induced ferroptosis in human pulmonary arterial smooth muscle cells. Under hypoxic conditions, ca-circSCN8A recruited EP300 to facilitate the lactylation of FUS (Fused in Sarcoma), triggering the formation of a ca-circSCN8A/FUS/EP300 complex via liquid-liquid phase separation. Liquid-liquid phase separation maintained the stability of the R-loop formed by ca-circSCN8A and ferroptosis-related gene SLC7A11 (solute carrier family 7 member 11) promoter that inhibits its transcription, further result in the disruption of the redox homeostasis and causing ferroptosis in human pulmonary arterial smooth muscle cells.</p><p><strong>Conclusions: </strong>ca-circSCN8A recruits EP300 to promote the lactylation of FUS, thereby driving liquid-liquid phase separation-mediated complex formation with FUS and EP300. This process enables ca-circSCN8A to form an R-loop with the nonhost SLC7A11 promoter, contributing to the regulation of hypoxia-induced ferroptosis in human pulmonary arterial smooth muscle cells. This study provides the first evidence that circRNAs can form R-loops with nonhost genes in a liquid-liquid phase separation-dependent manner. Our findings highlight ca-circSCN8A as a crucial regulator of ferroptosis in hypoxic PH and a potential therapeutic target for PH.</p>","PeriodicalId":13042,"journal":{"name":"Hypertension","volume":" ","pages":"e114-e128"},"PeriodicalIF":6.9,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144093387","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":"Regulatory Roles of Long Noncoding RNAs in Arterial Stiffness and Hypertension.","authors":"Jose D Vargas, Malak Abbas, Gabriel Goodney, Han Le, Antentor O Hinton, Amadou Gaye","doi":"10.1161/HYPERTENSIONAHA.124.23580","DOIUrl":"10.1161/HYPERTENSIONAHA.124.23580","url":null,"abstract":"<p><strong>Background: </strong>Arterial stiffness, commonly assessed via pulse wave velocity (PWV), is marked by reduced arterial elasticity and serves as a significant risk factor for cardiovascular disease and an early indicator of hypertension. This study investigated the regulatory roles of long noncoding RNAs (lncRNAs) in modulating mRNAs associated with arterial stiffness and hypertension, with a particular focus on African American individuals, a population disproportionately impacted by hypertension.</p><p><strong>Methods: </strong>We utilized whole-blood transcriptome sequencing data from 2 African American cohorts with high hypertension prevalence: the GENE-FORECAST (the Genomics, Environmental Factors, and Social Determinants of Cardiovascular Disease in African Americans Study; 436 subjects) and the MH-GRID study (Minority Health Genomics and Translational Research Bio-Repository Database; 179 subjects). Our objectives were to: (1) identify lncRNAs and mRNAs differentially expressed between the upper and lower tertiles of PWV; (2) determine differentially expressed lncRNAs associated with the expression levels of each differentially expressed mRNA; and (3) link the lncRNA-modulated mRNAs to hypertension across both data sets. For each of the 3 analyses, results were considered significant if the false discovery rate-adjusted <i>P</i> value was ≤0.05 in the discovery data set, the <i>P</i> value was ≤0.05 in the validation data set, and the effect size was consistent in direction across the 2 data sets.</p><p><strong>Results: </strong>Differential expression analysis revealed, respectively 1035 mRNAs and 31 lncRNAs differentially expressed between upper and lower PWV groups. Then, lncRNA-mRNA pairs significantly associated were identified, involving 31 unique lncRNAs and 1034 unique mRNAs. Finally, 22 of the lncRNA-modulated mRNAs initially linked to PWV were found to be associated with hypertension and replicated. Interestingly, 30 lncRNAs were linked to the expression of <i>UCP2</i> (Uncoupling Protein 2), a gene implicated in oxidative stress and endothelial function.</p><p><strong>Conclusions: </strong>Our findings underscore the significant roles of lncRNAs in regulating gene expression associated with arterial stiffness and hypertension. The differential expression of <i>UCP2</i> in relation to PWV and hypertension, along with its potential regulation by lncRNAs, offers valuable insights into the molecular mechanisms underlying arterial stiffness and its connection with hypertension.</p>","PeriodicalId":13042,"journal":{"name":"Hypertension","volume":" ","pages":"1195-1207"},"PeriodicalIF":6.9,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12178164/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144173758","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":"Sympathetic Vasomotion Reflects Catheter-Based Radiofrequency Renal Denervation.","authors":"Peter Ricci Pellegrino, Irving H Zucker, Yiannis S Chatzizisis, Han-Jun Wang, Alicia M Schiller","doi":"10.1161/HYPERTENSIONAHA.125.24980","DOIUrl":"10.1161/HYPERTENSIONAHA.125.24980","url":null,"abstract":"<p><strong>Background: </strong>The field of renal denervation remains challenged by the inability to confirm successful ablation of the targeted renal sympathetic nerves. The availability of technology to measure regional blood flow in real-time makes sympathetic control of the renal vasculature a logical end point to assess effective renal denervation, but autoregulatory mechanisms mask effects on mean renal blood flow. We hypothesized that renal sympathetic vasomotion, a novel marker of rhythmic sympathetic control, reflects successive rounds of catheter-based radiofrequency renal denervation.</p><p><strong>Methods: </strong>To test this, 10 pigs underwent unilateral surgical renal denervation, recovered for at least 7 days, and then underwent 4 successive rounds of catheter-based radiofrequency denervation of the contralateral kidney. Bilateral renal blood flow velocity and abdominal aortic pressure were measured before and after ablations to calculate renal vasomotion.</p><p><strong>Results: </strong>Before catheter-based denervation, the renal vasomotion profiles of the innervated and surgically denervated kidneys differed significantly (<i>P</i><0.005). Ablation of the largest renal branch artery reduced renal sympathetic vasomotion by 52%. Ablation of the remaining renal branch arteries reduced sympathetic vasomotion by 95% from baseline and eliminated the statistical differences between surgically and catheter-denervated kidneys. Two additional rounds of catheter denervation of the main renal artery did not consistently decrease the renal sympathetic vasomotion magnitude any further.</p><p><strong>Conclusions: </strong>These results indicate that renal sympathetic vasomotion could provide intraprocedural feedback for interventionalists performing catheter-based renal denervation and thereby improve the efficacy, safety, and consistency of this antihypertensive intervention.</p>","PeriodicalId":13042,"journal":{"name":"Hypertension","volume":" ","pages":"1261-1270"},"PeriodicalIF":6.9,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144150297","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":"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/HYPERTENSIONAHA.125.25045","DOIUrl":"10.1161/HYPERTENSIONAHA.125.25045","url":null,"abstract":"<p><strong>Background: </strong>Selective ablation of CUL3 (Cullin-3) in vascular smooth muscle cell-selective CUL3 knockout (S-CUL3KO) results in severe hypertension with paradoxically unaltered ANG II (angiotensin II) levels, suggesting an increase in ANG II sensitivity. We hypothesized that the hypertension and vascular dysfunction in S-CUL3KO mice are mediated by an exaggerated calcium response to ANG II in vascular smooth muscle cells.</p><p><strong>Methods: </strong>Blood pressure was measured by radiotelemetry in S-CUL3KO mice subjected to pharmacological inhibition of the renin-angiotensin system. Vascular function was evaluated in several arterial beds, and freshly isolated smooth muscle cells were used to elucidate the contribution of CUL3 to ANG II-induced cytosolic calcium concentration flux. The involvement of potential calcium channels was evaluated based on gene expression in carotid arteries and pharmacological studies.</p><p><strong>Results: </strong>S-CUL3KO mice exhibited severe hypertension with an enhanced depressor response following the administration of renin-angiotensin system inhibitors. Candesartan administration before induction of the CUL3 deletion revealed both nonrenin-angiotensin system and renin-angiotensin system components to the development of hypertension. Increased ANG II-induced vasoconstriction was observed in mesenteric and basilar arteries in S-CUL3KO mice. Freshly isolated smooth muscle cells from S-CUL3KO exhibited an excessive cytosolic calcium concentration flux in response to ANG II. Gene expression studies of carotid arteries from S-CUL3KO mice led us to hypothesize a potential role for TRPC6 (Transient Receptor Potential Cation Channel Subfamily C Member 6) in ANG II hyperresponsiveness. TRPC6 pharmacological inhibition blunted the exaggerated ANG II-induced cytosolic calcium concentration flux in smooth muscle cells, blunted ANG II-induced vasoconstriction and lowered blood pressure in S-CUL3KO mice.</p><p><strong>Conclusions: </strong>Collectively, these data are consistent with the conclusion that loss of CUL3 function enhances ANG II sensitivity by increasing TRPC6-mediated cytosolic calcium concentration flux in smooth muscle cells.</p>","PeriodicalId":13042,"journal":{"name":"Hypertension","volume":" ","pages":"1208-1220"},"PeriodicalIF":6.9,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12176512/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144180112","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":"Drinking Water NaCl Is Associated With Hypertension and Albuminuria: A Panel Study.","authors":"Asher Y Rosinger,Amanda McGrosky,Hannah Jacobson,Elena Hinz,Srishti Sadhir,Faith Wambua,Tom Otube,Lilian Baker,Alison Sherwood,Tiffany Chrissy-Mbeng,Lauren Broyles,Carey Musumeci,Natalie Meriwether,Nicole Bobbie,Zoë Farrar,Madeleine Todd,Zee Nguyen,Gabriella Berger,Leslie B Ford,David R Braun,Michael D Hunter,Matthew Douglass,William Farquhar,W Larry Kenney,Jeff M Sands,Rosemary Nzunza,Emmanuel Ndiema,Herman Pontzer","doi":"10.1161/hypertensionaha.125.24751","DOIUrl":"https://doi.org/10.1161/hypertensionaha.125.24751","url":null,"abstract":"BACKGROUNDSalt leaching into freshwater is an emerging global environmental health concern. We tested the associations between drinking water salinity and blood pressure, hypertension, and albuminuria.METHODSWe conducted a 2-year panel study in 2022 and 2023 with 434 observations among 327 Daasanach adults aged >18 years in northern Kenya. Water sources were analyzed for overall salinity and ionic composition (sodium-chloride; calcium, potassium, magnesium). We measured resting blood pressure and classified hypertension stage 1 and stage 2. Urine samples were analyzed for albuminuria (≥30 mg/g albumin-to-creatinine ratio).RESULTSDrinking water salinity was driven by sodium-chloride (mean=162.6 mg/L, SD=77.1), with low concentrations of calcium, potassium, and magnesium (mean=45 mg/L, SD=13.5). Across 2022 and 2023, 40.1% of adults had at least hypertension stage 1, 13.5% had hypertension stage 2, and 42.2% had albuminuria. Using random effects linear and logistic panel regressions fully adjusted for confounders, each 100 mg/L of drinking water sodium-chloride was associated with 4.5 mm Hg (95% CI, 2.4-6.6) and 3.3 mm Hg (95% CI, 2.2-4.5) increases in systolic and diastolic blood pressure, 3.0× the odds of at least hypertension stage 1 (95% CI, 1.49-5.83), 3.6× the odds of hypertension stage 2 (95% CI, 1.93-6.81), and 2.0× the odds of albuminuria (95% CI, 1.28-3.06). Calcium, potassium, and magnesium were unassociated with any outcomes. Hypertension stage 2 (but not hypertension stage 1) was associated with 2.6× (95% CI, 1.19-5.77) the odds of albuminuria.CONCLUSIONSDrinking water sodium-chloride was associated with resting blood pressure, hypertension, and albuminuria in a population with few traditional lifestyle risk factors for chronic disease. Measuring specific salts in water helps untangle associations with hypertension.","PeriodicalId":13042,"journal":{"name":"Hypertension","volume":"16 1","pages":""},"PeriodicalIF":8.3,"publicationDate":"2025-06-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144370268","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":"Macrophage-Derived LCN2 Promotes Methamphetamine-Induced Pulmonary Hypertension.","authors":"Jie Zhou, Zhenzhen Xu, Dao-Bo Peng, Xiaoting Li, Sheng Chang, Ke Duan, Yating Jiang, Cihang Gu, Xiaojia Peng, Wei-Bing Xie","doi":"10.1161/HYPERTENSIONAHA.124.24548","DOIUrl":"https://doi.org/10.1161/HYPERTENSIONAHA.124.24548","url":null,"abstract":"<p><strong>Background: </strong>Methamphetamine (METH), a novel amphetamine-type psychostimulant, is recognized as a risk factor for pulmonary hypertension (PH). Macrophage activation is a key event in pulmonary vascular remodeling and PH progression, but the specific mechanisms of METH-induced PH (METH-PH) remain unclear.</p><p><strong>Methods: </strong>A METH-PH mouse model was constructed using wild-type and Lipocalin 2 (LCN2) knockout (LCN2^-/-) mice. The involvement and underlying mechanism of LCN2 in METH-PH formation were explored using a METH-PH mouse model and a coculture system of macrophages and pulmonary artery smooth muscle cells.</p><p><strong>Results: </strong>In this study, LCN2 was identified as a key regulator of perivascular inflammation and pulmonary vascular remodeling in PH. In the METH-PH mouse model, LCN2 expression was elevated in macrophages within lung tissues. Compared with wild-type mice, LCN2^-/- mice were protected from METH-PH, exhibiting reduced pulmonary vascular remodeling and right ventricular pressure. Mechanistically, LCN2 regulates IL-1β (interleukin-1β) production and secretion through NLRP3 (NOD-, LRR-, and pyrin domain-containing protein 3) inflammasome activation. In pulmonary artery smooth muscle cells, macrophage-derived LCN2 upregulates the expression of SLC7A11 (solute carrier family 7 member 11) and GPX4 (glutathione peroxidase 4), thereby reducing reactive oxygen species production and preventing ferroptosis.</p><p><strong>Conclusions: </strong>Our data revealed a novel mechanism linking LCN2 to macrophages, inflammatory responses, vascular remodeling, and intercellular interactions, indicating that LCN2 could serve as a therapeutic target for METH-induced PH.</p>","PeriodicalId":13042,"journal":{"name":"Hypertension","volume":" ","pages":""},"PeriodicalIF":6.9,"publicationDate":"2025-06-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144368818","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":"TGFβ Superfamily in Pulmonary Vascular Disease: The Role of SMAD4.","authors":"John A Baugh,Paul McLoughlin","doi":"10.1161/hypertensionaha.125.25020","DOIUrl":"https://doi.org/10.1161/hypertensionaha.125.25020","url":null,"abstract":"","PeriodicalId":13042,"journal":{"name":"Hypertension","volume":"3 1","pages":"1192-1194"},"PeriodicalIF":8.3,"publicationDate":"2025-06-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144320086","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":"Correction to: Disparities in Postpartum Care After a Hypertensive Disorder of Pregnancy in the United States.","authors":"Megan M McLaughlin,Neda Ghaffari,Catherine Lee,Malamo E Countouris,Phoebe Ashley,Amanda Schnell Heringer","doi":"10.1161/hyp.0000000000000246","DOIUrl":"https://doi.org/10.1161/hyp.0000000000000246","url":null,"abstract":"","PeriodicalId":13042,"journal":{"name":"Hypertension","volume":"44 1","pages":"e141"},"PeriodicalIF":8.3,"publicationDate":"2025-06-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144319754","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":"In Memoriam: Stevo Julius, MD, ScD.","authors":"Sverre E Kjeldsen,Murray Esler,Kenneth A Jamerson,Brent Egan,Giuseppe Mancia","doi":"10.1161/hypertensionaha.125.25152","DOIUrl":"https://doi.org/10.1161/hypertensionaha.125.25152","url":null,"abstract":"","PeriodicalId":13042,"journal":{"name":"Hypertension","volume":"147 1","pages":"e110-e113"},"PeriodicalIF":8.3,"publicationDate":"2025-06-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144320090","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}