Pub Date : 2025-12-29DOI: 10.1161/hypertensionaha.125.25803
Xiaobin Han,Zhongjie Sun
BACKGROUNDAlthough epigenetic modification of histone in embryonic development is well documented, its mechanistic role in the pathogenesis of hypertension is poorly understood. The purpose of this study is to investigate how histone 3 modification (H3K27me3 [trimethylation of histone 3 lysine 27]) in renal tubule cells regulates sodium excretion and blood pressure.METHODSA mouse model of inducible renal tubule cell-specific deletion of KDM6A cKO (histone 3 lysine 27 demethylase 6A gene) was generated.RESULTSHere, we uncovered the potential role of FBLN2 (fibulin 2) in the pathogenesis of epigenetic hypertension due to KDM6A cKO. KDM6A is a specific demethylase for H3K27me3. ChIP-seq analysis revealed that the H3K27me3 mark was increased in the promoter region of the FBLN2 gene, resulting in downregulation of FBLN2 protein expression in the kidney of KDM6A cKO mice. Treatment with rFBLN2 (recombinant FBLN2) largely attenuated blood pressure elevation, rescued impairment in sodium excretion, and prevented high salt-induced salt-sensitive hypertension in KDM6A cKO mice. Mechanistically, treatment with rFBLN2 rescued upregulation of NCC (Na-Cl cotransporter) and AQP2 (aquaporin 2) expression and decreased NKCC2 expression in renal tubular cells in the KDM6A cKO hypertensive mice. Intriguingly, FBLN2 may regulate NCC trafficking via forming an FBLN2/NCC complex, which decreases the cell membrane abundance of NCC by translocating NCC to the total membrane in distal convoluted tubule cells.CONCLUSIONSThese findings highlight a critical role of FBLN2 in the regulation of renal sodium excretion and blood pressure and suggest that FBLN2 deficiency may drive KDM6A deficiency-induced epigenetic hypertension. FBLN2 treatment may provide a new preventive and therapeutic strategy for salt-sensitive hypertension.
{"title":"Fibulin 2 Deficiency Drives Epigenetic Hypertension.","authors":"Xiaobin Han,Zhongjie Sun","doi":"10.1161/hypertensionaha.125.25803","DOIUrl":"https://doi.org/10.1161/hypertensionaha.125.25803","url":null,"abstract":"BACKGROUNDAlthough epigenetic modification of histone in embryonic development is well documented, its mechanistic role in the pathogenesis of hypertension is poorly understood. The purpose of this study is to investigate how histone 3 modification (H3K27me3 [trimethylation of histone 3 lysine 27]) in renal tubule cells regulates sodium excretion and blood pressure.METHODSA mouse model of inducible renal tubule cell-specific deletion of KDM6A cKO (histone 3 lysine 27 demethylase 6A gene) was generated.RESULTSHere, we uncovered the potential role of FBLN2 (fibulin 2) in the pathogenesis of epigenetic hypertension due to KDM6A cKO. KDM6A is a specific demethylase for H3K27me3. ChIP-seq analysis revealed that the H3K27me3 mark was increased in the promoter region of the FBLN2 gene, resulting in downregulation of FBLN2 protein expression in the kidney of KDM6A cKO mice. Treatment with rFBLN2 (recombinant FBLN2) largely attenuated blood pressure elevation, rescued impairment in sodium excretion, and prevented high salt-induced salt-sensitive hypertension in KDM6A cKO mice. Mechanistically, treatment with rFBLN2 rescued upregulation of NCC (Na-Cl cotransporter) and AQP2 (aquaporin 2) expression and decreased NKCC2 expression in renal tubular cells in the KDM6A cKO hypertensive mice. Intriguingly, FBLN2 may regulate NCC trafficking via forming an FBLN2/NCC complex, which decreases the cell membrane abundance of NCC by translocating NCC to the total membrane in distal convoluted tubule cells.CONCLUSIONSThese findings highlight a critical role of FBLN2 in the regulation of renal sodium excretion and blood pressure and suggest that FBLN2 deficiency may drive KDM6A deficiency-induced epigenetic hypertension. FBLN2 treatment may provide a new preventive and therapeutic strategy for salt-sensitive hypertension.","PeriodicalId":13042,"journal":{"name":"Hypertension","volume":"68 1","pages":""},"PeriodicalIF":8.3,"publicationDate":"2025-12-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145847207","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}
BACKGROUNDWhite matter hyperintensities (WMH), a hallmark imaging feature of small vessel disease, are strongly associated with neurodegenerative and cardiovascular conditions.METHODSWe performed bidirectional and mediation Mendelian randomization analyses using summary statistics from GWAS (genome-wide association studies) of 9 large cohorts of plasma proteins (n=997-35 559), blood pressure (n=1 028 980), and WMH (n=21 381). The inverse-variance-weighted method or Wald ratio was applied as the primary Mendelian randomization approach, with false discovery rate correction and independent replication. We further integrated Mendelian randomization with PheWAS (phenome-wide association studies) to prioritize WMH risk factors and assess mediation via systolic blood pressure and diastolic blood pressure.RESULTSEighteen plasma proteins were genetically associated with WMH, 13 of which were replicated. Thirteen antihypertensive target genes were also linked to WMH burden, including ADRB3, AOC1 (amine oxidase copper containing 1), SHBG (sex hormone binding blobulin), and KCNH2 (potassium voltage-gated channel subfamily H member 2), which influenced both systolic blood pressure and diastolic blood pressure. Mendelian randomization-PheWAS highlighted systolic blood pressure and diastolic blood pressure as the top-ranked WMH risk factors among 21 976 traits. Antihypertensive drug targets, including angiotensin II receptor blockers, β-blockers, calcium channel blockers, and diuretics, were significantly associated with WMH burden. Mediation analysis showed that systolic blood pressure partially mediated TFPI's effect (3.04%), and diastolic blood pressure mediated the effects of ACP1 (acid phosphatase 1) (2.74%) and LAMC1 (laminin subunit gamma 1; 4.94%).CONCLUSIONSThe findings outline protein- and blood pressure-centered mechanisms in small vessel disease, highlighting proteins and antihypertensive targets as biomarkers and therapeutic entry points for precision intervention.
{"title":"Genetic Dissection of Plasma Proteins and Blood Pressure in Small Vessel Disease.","authors":"Yaoyao Yu,Tianyi Xia,Yinlu Wang,Keli Qin,Lingling Gao,Ben Zhao,Junhao Zha,Jiaying Zhou,Ying Cui,Chunqiang Lu,Tianyu Tang,Zebin Xiao,Shenghong Ju","doi":"10.1161/hypertensionaha.125.25608","DOIUrl":"https://doi.org/10.1161/hypertensionaha.125.25608","url":null,"abstract":"BACKGROUNDWhite matter hyperintensities (WMH), a hallmark imaging feature of small vessel disease, are strongly associated with neurodegenerative and cardiovascular conditions.METHODSWe performed bidirectional and mediation Mendelian randomization analyses using summary statistics from GWAS (genome-wide association studies) of 9 large cohorts of plasma proteins (n=997-35 559), blood pressure (n=1 028 980), and WMH (n=21 381). The inverse-variance-weighted method or Wald ratio was applied as the primary Mendelian randomization approach, with false discovery rate correction and independent replication. We further integrated Mendelian randomization with PheWAS (phenome-wide association studies) to prioritize WMH risk factors and assess mediation via systolic blood pressure and diastolic blood pressure.RESULTSEighteen plasma proteins were genetically associated with WMH, 13 of which were replicated. Thirteen antihypertensive target genes were also linked to WMH burden, including ADRB3, AOC1 (amine oxidase copper containing 1), SHBG (sex hormone binding blobulin), and KCNH2 (potassium voltage-gated channel subfamily H member 2), which influenced both systolic blood pressure and diastolic blood pressure. Mendelian randomization-PheWAS highlighted systolic blood pressure and diastolic blood pressure as the top-ranked WMH risk factors among 21 976 traits. Antihypertensive drug targets, including angiotensin II receptor blockers, β-blockers, calcium channel blockers, and diuretics, were significantly associated with WMH burden. Mediation analysis showed that systolic blood pressure partially mediated TFPI's effect (3.04%), and diastolic blood pressure mediated the effects of ACP1 (acid phosphatase 1) (2.74%) and LAMC1 (laminin subunit gamma 1; 4.94%).CONCLUSIONSThe findings outline protein- and blood pressure-centered mechanisms in small vessel disease, highlighting proteins and antihypertensive targets as biomarkers and therapeutic entry points for precision intervention.","PeriodicalId":13042,"journal":{"name":"Hypertension","volume":"23 1","pages":""},"PeriodicalIF":8.3,"publicationDate":"2025-12-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145847327","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}
Pub Date : 2025-12-29DOI: 10.1161/hypertensionaha.124.25516
Katherine N Theken,Soumita Ghosh,Carsten Skarke,Susanne Fries,Nicholas F Lahens,Dimitra Sarantopoulou,Gregory R Grant,Garret A FitzGerald,Tilo Grosser
BACKGROUNDLarge clinical trials compared distinct nonsteroidal anti-inflammatory drugs in terms of their risk of adverse cardiovascular events. However, whether pharmacologically equipotent doses were used, that is, whether a similar degree of COX (cyclooxygenase)-2 inhibition was achieved, was not considered. We compared drug target inhibition and blood pressure (BP) response to celecoxib and naproxen.METHODSSixteen healthy participants were treated with celecoxib (200 mg/d), naproxen (500 mg/d), or placebo for 7 days in a double-blind, crossover design. The degree of COX inhibition was assessed ex vivo using established whole blood assays and in vivo by quantifying urinary metabolites of thromboxane A2 (COX-1) and prostacyclin (COX-2). Ambulatory BP was measured throughout the final dosing interval.RESULTSBoth nonsteroidal anti-inflammatory drugs inhibited COX-2 activity relative to placebo, but naproxen inhibited COX-2 activity to a greater degree (62.9±21.7%) than celecoxib (35.7±25.2%; P<0.05). Similarly, naproxen treatment inhibited prostacyclin formation in vivo (48.0±24.9%) to a greater degree than celecoxib (26.7±24.6%; P<0.05). Naproxen significantly increased BP compared with celecoxib (mean arterial pressure, 2.5 [95% CI, 1.5-3.5] mm Hg; systolic BP, 4.0 [95% CI, 2.9-5.1] mm Hg; and diastolic BP, 1.8 [95% CI, 0.8-2.8] mm Hg; P<0.05 for all). The difference in systolic BP relative to placebo was associated with the degree of COX-2 inhibition (P<0.05).CONCLUSIONSFuture studies should consider pharmacokinetic and pharmacodynamic properties, as well as patient-specific factors that may modulate the cardiovascular risk of nonsteroidal anti-inflammatory drug use.
背景：大型临床试验比较了不同的非甾体类抗炎药的不良心血管事件风险。然而，没有考虑是否使用药理学上等效的剂量，即是否达到相似程度的COX（环氧化酶）-2抑制。我们比较了塞来昔布和萘普生的药物靶标抑制和血压（BP）反应。方法采用双盲交叉设计，16名健康受试者接受塞来昔布（200 mg/d）、萘普生（500 mg/d）或安慰剂治疗7天。在体外通过建立全血测定法评估COX抑制程度，在体内通过量化血栓素A2 （COX-1）和前列环素（COX-2）的尿液代谢物来评估COX抑制程度。在最后给药期间测量动态血压。结果两种非甾体类抗炎药均较安慰剂抑制COX-2活性，但萘普生抑制COX-2活性的程度（62.9±21.7%）高于塞来昔布（35.7±25.2%，P<0.05）。同样，萘普生对体内前列环素形成的抑制程度（48.0±24.9%）高于塞来昔布（26.7±24.6%，P<0.05）。与塞来昔布相比，萘普生显著升高血压（平均动脉压，2.5 [95% CI, 1.5-3.5] mm Hg；收缩压，4.0 [95% CI, 2.9-5.1] mm Hg；舒张压，1.8 [95% CI, 0.8-2.8] mm Hg； P<0.05）。收缩压与安慰剂的差异与COX-2抑制程度相关（P<0.05）。结论未来的研究应考虑药代动力学和药效学特性，以及可能调节非甾体抗炎药使用心血管风险的患者特异性因素。
{"title":"Degree of Cyclooxygenase-2 Inhibition Modulates Blood Pressure Response.","authors":"Katherine N Theken,Soumita Ghosh,Carsten Skarke,Susanne Fries,Nicholas F Lahens,Dimitra Sarantopoulou,Gregory R Grant,Garret A FitzGerald,Tilo Grosser","doi":"10.1161/hypertensionaha.124.25516","DOIUrl":"https://doi.org/10.1161/hypertensionaha.124.25516","url":null,"abstract":"BACKGROUNDLarge clinical trials compared distinct nonsteroidal anti-inflammatory drugs in terms of their risk of adverse cardiovascular events. However, whether pharmacologically equipotent doses were used, that is, whether a similar degree of COX (cyclooxygenase)-2 inhibition was achieved, was not considered. We compared drug target inhibition and blood pressure (BP) response to celecoxib and naproxen.METHODSSixteen healthy participants were treated with celecoxib (200 mg/d), naproxen (500 mg/d), or placebo for 7 days in a double-blind, crossover design. The degree of COX inhibition was assessed ex vivo using established whole blood assays and in vivo by quantifying urinary metabolites of thromboxane A2 (COX-1) and prostacyclin (COX-2). Ambulatory BP was measured throughout the final dosing interval.RESULTSBoth nonsteroidal anti-inflammatory drugs inhibited COX-2 activity relative to placebo, but naproxen inhibited COX-2 activity to a greater degree (62.9±21.7%) than celecoxib (35.7±25.2%; P<0.05). Similarly, naproxen treatment inhibited prostacyclin formation in vivo (48.0±24.9%) to a greater degree than celecoxib (26.7±24.6%; P<0.05). Naproxen significantly increased BP compared with celecoxib (mean arterial pressure, 2.5 [95% CI, 1.5-3.5] mm Hg; systolic BP, 4.0 [95% CI, 2.9-5.1] mm Hg; and diastolic BP, 1.8 [95% CI, 0.8-2.8] mm Hg; P<0.05 for all). The difference in systolic BP relative to placebo was associated with the degree of COX-2 inhibition (P<0.05).CONCLUSIONSFuture studies should consider pharmacokinetic and pharmacodynamic properties, as well as patient-specific factors that may modulate the cardiovascular risk of nonsteroidal anti-inflammatory drug use.","PeriodicalId":13042,"journal":{"name":"Hypertension","volume":"183 1","pages":""},"PeriodicalIF":8.3,"publicationDate":"2025-12-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145847254","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}
Pub Date : 2025-12-18DOI: 10.1161/hypertensionaha.125.26149
Peeradon Vibhatavata,Livia M Mermejo,Lili Zhao,James J Shields,Adina F Turcu
BACKGROUNDAdrenal vein (AV) sampling (AVS) is used to guide therapy in primary aldosteronism (PA). When a single AV is successfully cannulated, the relative aldosterone secretion index (RASI), which compares the aldosterone/cortisol ratio in that AV versus the periphery, has been proposed as sufficient for PA subtyping, particularly when <1. Data on RASI reliability have, however, been inconsistent.METHODSThis retrospective cohort study included patients with PA who underwent AVS before and after cosyntropin stimulation at a referral center between January 2015 and December 2024. To simulate partially successful AVS, RASI was calculated from patients with successful bilateral AV cannulation and compared across PA subtypes and postoperative outcomes, with assessment of distributional overlap.RESULTSOf 460 patients (mean age 53±12 years; 58% men), bilateral AVS was successful in 437 patients at baseline and in all patients after cosyntropin stimulation. Without cosyntropin, 98% of dominant AV and 97% of nondominant AV RASI from lateralized PA overlapped with bilateral PA RASI. Similar patterns were observed postcosyntropin. In adrenalectomized patients, RASI did not distinguish between those with and without PA cure. Previously proposed RASI thresholds misclassified up to 74% of lateralized PA and 64% of bilateral PA. When corroborated with cross-sectional imaging, the prediction of correct lateralization improved, particularly when using RASI from cosyntropin-stimulated AVS.CONCLUSIONSConsidering the substantial overlap of RASI across PA subtypes, partially successful AVS has limited utility and is unreliable in guiding adrenalectomy for PA.
{"title":"Partially Successful Adrenal Vein Sampling With and Without Cross-Sectional Imaging in Primary Aldosteronism Subtyping.","authors":"Peeradon Vibhatavata,Livia M Mermejo,Lili Zhao,James J Shields,Adina F Turcu","doi":"10.1161/hypertensionaha.125.26149","DOIUrl":"https://doi.org/10.1161/hypertensionaha.125.26149","url":null,"abstract":"BACKGROUNDAdrenal vein (AV) sampling (AVS) is used to guide therapy in primary aldosteronism (PA). When a single AV is successfully cannulated, the relative aldosterone secretion index (RASI), which compares the aldosterone/cortisol ratio in that AV versus the periphery, has been proposed as sufficient for PA subtyping, particularly when <1. Data on RASI reliability have, however, been inconsistent.METHODSThis retrospective cohort study included patients with PA who underwent AVS before and after cosyntropin stimulation at a referral center between January 2015 and December 2024. To simulate partially successful AVS, RASI was calculated from patients with successful bilateral AV cannulation and compared across PA subtypes and postoperative outcomes, with assessment of distributional overlap.RESULTSOf 460 patients (mean age 53±12 years; 58% men), bilateral AVS was successful in 437 patients at baseline and in all patients after cosyntropin stimulation. Without cosyntropin, 98% of dominant AV and 97% of nondominant AV RASI from lateralized PA overlapped with bilateral PA RASI. Similar patterns were observed postcosyntropin. In adrenalectomized patients, RASI did not distinguish between those with and without PA cure. Previously proposed RASI thresholds misclassified up to 74% of lateralized PA and 64% of bilateral PA. When corroborated with cross-sectional imaging, the prediction of correct lateralization improved, particularly when using RASI from cosyntropin-stimulated AVS.CONCLUSIONSConsidering the substantial overlap of RASI across PA subtypes, partially successful AVS has limited utility and is unreliable in guiding adrenalectomy for PA.","PeriodicalId":13042,"journal":{"name":"Hypertension","volume":"1 1","pages":""},"PeriodicalIF":8.3,"publicationDate":"2025-12-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145771390","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}
Pub Date : 2025-12-17DOI: 10.1161/hypertensionaha.125.25719
Joseph E Ebinger,Anni Kauko,Felix Vaura,Paul Hage,Johan Sundström,Sandy Y Joung,Susan Cheng,Teemu Niiranen,
BACKGROUNDResistant hypertension (RH), in which blood pressure remains elevated on ≥3 medications or controlled on ≥4 medications, increases the risk of adverse cardiovascular events nearly 50% more than primary hypertension. We sought to identify genetic drivers of RH in a reliable and generalizable manner.METHODSWe utilized FinnGen (discovery) and UKBB (UK Biobank, replication) data sets to identify potential genetic drivers of RH. Using standard RH definitions, we developed cohorts in each data set and performed genome-wide (genome-wide association studies) and transcriptome-wide association studies, as well as Mendelian randomization analysis to evaluate potential causal associations.RESULTSWe replicated 5 genetic loci in CASZ1, WNT2B, KCNK3, LSP1, and near the EVX1/EVX1AS locus for RH. Of these, CASZ1 and WNT2B are strongly associated with aldosterone homeostasis, while KCNK3 and LSP1 are associated with pathways mediating vasodilation. EVX1/EVX1AS are involved in mesendodermal lineage differentiation during gastrulation. Gene- and pathway-based analyses identified associations with vascular and cardiac developmental pathways in addition to aldosterone synthesis and secretion pathways. Transcriptome-wide association study analyses identified 37 genes, of which the genetically regulated expression is associated with RH, with particularly strong tissue-specific associations with KCNK3. Finally, Mendelian randomization identified possible causal association for 4 vascular risk factors (CRP [C-reactive protein]), triglycerides, waist circumference, and body mass index) with RH, with strong associations with identified lead variants.CONCLUSIONSWe identified distinct genetic variants associated with RH, including those implicating the role of hyperaldosteronism, highlighting distinct pathways and targets for more effectively treating RH.
{"title":"GWAS and Replication Analysis of Apparent Treatment-Resistant Hypertension.","authors":"Joseph E Ebinger,Anni Kauko,Felix Vaura,Paul Hage,Johan Sundström,Sandy Y Joung,Susan Cheng,Teemu Niiranen, ","doi":"10.1161/hypertensionaha.125.25719","DOIUrl":"https://doi.org/10.1161/hypertensionaha.125.25719","url":null,"abstract":"BACKGROUNDResistant hypertension (RH), in which blood pressure remains elevated on ≥3 medications or controlled on ≥4 medications, increases the risk of adverse cardiovascular events nearly 50% more than primary hypertension. We sought to identify genetic drivers of RH in a reliable and generalizable manner.METHODSWe utilized FinnGen (discovery) and UKBB (UK Biobank, replication) data sets to identify potential genetic drivers of RH. Using standard RH definitions, we developed cohorts in each data set and performed genome-wide (genome-wide association studies) and transcriptome-wide association studies, as well as Mendelian randomization analysis to evaluate potential causal associations.RESULTSWe replicated 5 genetic loci in CASZ1, WNT2B, KCNK3, LSP1, and near the EVX1/EVX1AS locus for RH. Of these, CASZ1 and WNT2B are strongly associated with aldosterone homeostasis, while KCNK3 and LSP1 are associated with pathways mediating vasodilation. EVX1/EVX1AS are involved in mesendodermal lineage differentiation during gastrulation. Gene- and pathway-based analyses identified associations with vascular and cardiac developmental pathways in addition to aldosterone synthesis and secretion pathways. Transcriptome-wide association study analyses identified 37 genes, of which the genetically regulated expression is associated with RH, with particularly strong tissue-specific associations with KCNK3. Finally, Mendelian randomization identified possible causal association for 4 vascular risk factors (CRP [C-reactive protein]), triglycerides, waist circumference, and body mass index) with RH, with strong associations with identified lead variants.CONCLUSIONSWe identified distinct genetic variants associated with RH, including those implicating the role of hyperaldosteronism, highlighting distinct pathways and targets for more effectively treating RH.","PeriodicalId":13042,"journal":{"name":"Hypertension","volume":"50 1","pages":""},"PeriodicalIF":8.3,"publicationDate":"2025-12-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145765394","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}
Pub Date : 2025-12-17DOI: 10.1161/hypertensionaha.125.26261
Stanislovas S Jankauskas,Urna Kansakar,Pasquale Mone,Fahimeh Varzideh,Gaetano Santulli
{"title":"Like a Rolling Tone: Ablating LRRC8A Eases Inflammation and Keeps Vessels Moving.","authors":"Stanislovas S Jankauskas,Urna Kansakar,Pasquale Mone,Fahimeh Varzideh,Gaetano Santulli","doi":"10.1161/hypertensionaha.125.26261","DOIUrl":"https://doi.org/10.1161/hypertensionaha.125.26261","url":null,"abstract":"","PeriodicalId":13042,"journal":{"name":"Hypertension","volume":"366 1","pages":"54-56"},"PeriodicalIF":8.3,"publicationDate":"2025-12-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145771553","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}
Pub Date : 2025-12-17DOI: 10.1161/hypertensionaha.125.26151
Olivier Steichen
{"title":"What It Takes for Food to Be Medicine: Lessons From the Rice Diet Era.","authors":"Olivier Steichen","doi":"10.1161/hypertensionaha.125.26151","DOIUrl":"https://doi.org/10.1161/hypertensionaha.125.26151","url":null,"abstract":"","PeriodicalId":13042,"journal":{"name":"Hypertension","volume":"21 1","pages":"37-39"},"PeriodicalIF":8.3,"publicationDate":"2025-12-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145771392","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}
Pub Date : 2025-12-17DOI: 10.1161/hypertensionaha.125.25649
Elizabeth Lemoine,Ravi Thadhani
{"title":"Pointing Care for Preeclampsia in the Right Direction.","authors":"Elizabeth Lemoine,Ravi Thadhani","doi":"10.1161/hypertensionaha.125.25649","DOIUrl":"https://doi.org/10.1161/hypertensionaha.125.25649","url":null,"abstract":"","PeriodicalId":13042,"journal":{"name":"Hypertension","volume":"153 1","pages":"23-25"},"PeriodicalIF":8.3,"publicationDate":"2025-12-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145771554","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}
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