Hypertension最新文献

{"title":"Reliability of Blood Pressure Measurement After Arteriovenous Fistula Closure in Kidney Transplant Recipients.","authors":"Yara Fares,Margaux Van Wynsberghe,Dominique Bertrand,Steven Grange,Charlotte Laurent,Dominique Guerrot,Tristan de Nattes","doi":"10.1161/hypertensionaha.125.25081","DOIUrl":"https://doi.org/10.1161/hypertensionaha.125.25081","url":null,"abstract":"","PeriodicalId":13042,"journal":{"name":"Hypertension","volume":"109 1","pages":"e154-e156"},"PeriodicalIF":8.3,"publicationDate":"2025-07-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144645842","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":"Constructing a Preeclampsia Organoid Model to Elucidate the Mechanism of Aspirin.","authors":"Shengbo Huang,Yuanjin Zhang,Yuanqing Guo,Yi Zhang,Junze Huang,Yujia Yang,Qifan Qi,Luping Zhao,Xin Xu,Yifei Shen,Chenmeizi Liang,Bingyi Yao,Xin Wang","doi":"10.1161/hypertensionaha.125.25342","DOIUrl":"https://doi.org/10.1161/hypertensionaha.125.25342","url":null,"abstract":"BACKGROUNDPreeclampsia is a life-threatening pregnancy disorder characterized by hypertension and multiorgan dysfunction, posing significant risks to both maternal and fetal health. Although low-dose aspirin is widely recommended for preventing preeclampsia, the underlying mechanisms of action are still poorly understood, which hinders the optimization of therapeutic strategies.METHODSWe developed an in vitro hypoxia-induced preeclampsia model using human trophoblast organoids to replicate key pathological features. RNA sequencing identified dysregulated pathways and molecular targets. Functional assays assessed the effects of aspirin on trophoblast proliferation, mitochondrial activity, and hormonal regulation, focusing on the PI3K-AKT pathway and CYP (cytochrome P450) enzymes. We also analyzed the effects of aspirin in the N'-nitro-L-arginine-methyl ester hydrochloride rat models.RESULTSThe hypoxia-induced preeclampsia model successfully mimicked clinical hallmarks, including elevated sFLT-1 (soluble fms-like tyrosine kinase 1)/PlGF (placental growth factor) ratios and oxidative damage. RNA sequencing revealed significant suppression of the PI3K-AKT-mTOR pathway and dysregulation of CYP enzymes. Aspirin treatment restored the sFLT-1/PlGF balance, reactivated the PI3K-AKT-mTOR pathway, and improved mitochondrial function, enhancing trophoblast proliferation. Furthermore, aspirin regulated CYP expression by increasing CYP19A1 and inhibiting CYP1A1, thereby improving placental hormonal homeostasis.CONCLUSIONSThis study clarifies aspirin's multitarget mechanisms in alleviating preeclampsia, which include restoring the sFLT-1/PlGF balance, activating the PI3K-AKT-mTOR signaling pathway, optimizing mitochondrial function, and regulating CYP-mediated hormonal metabolism. These findings provide a mechanistic basis for aspirin's clinical effectiveness in preventing preeclampsia.","PeriodicalId":13042,"journal":{"name":"Hypertension","volume":"27 1","pages":""},"PeriodicalIF":8.3,"publicationDate":"2025-07-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144640093","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":"Simplifications of the Standardized BP Measurement Procedure and Accuracy: The SIMPLE-AOBP Randomized Cross-Over Trial.","authors":"Rémi Goupil,Mérédith Lacasse,Dean S Picone","doi":"10.1161/hypertensionaha.125.25079","DOIUrl":"https://doi.org/10.1161/hypertensionaha.125.25079","url":null,"abstract":"","PeriodicalId":13042,"journal":{"name":"Hypertension","volume":"4 1","pages":"e157-e159"},"PeriodicalIF":8.3,"publicationDate":"2025-07-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144645843","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":"E-Cigarette Smoke Exposure Elevates Renal MR Expression and Induces BP Elevation.","authors":"Jian Wang,Bei Xu,Ying Wang,Jenny Liu,Piwen Wang,Rene Porche,Samuel Kim,Rong Yang,Xuesi M Shao,Kabirullah Lutfy,Limei Liu,Theodore C Friedman,Meisheng Jiang,Yanjun Liu","doi":"10.1161/hypertensionaha.124.23489","DOIUrl":"https://doi.org/10.1161/hypertensionaha.124.23489","url":null,"abstract":"BACKGROUNDE-cigarette use increases the risk of blood pressure (BP) elevation in users, though the underlying mechanisms remain unclear. The mineralocorticoid receptor (MR) is known to play an important role in the regulation of renal electrolyte balance and BP, and is protected by 11β-HSD2 (11β-hydroxysteroid dehydrogenase type 2). However, little is known about the effects of renal MR on e-cigarette-induced BP elevation.METHODSC57BL/6J male mice were exposed to aerosolized PBS, e-cigarettes without nicotine, and e-cigarettes with 2.4% nicotine, with concurrent exposure to either a vehicle or the MR antagonist eplerenone.RESULTSInhalation of e-cigarettes with nicotine markedly induced renal MR abundance and increased mean arterial BP in response to elevated plasma nicotine levels in C57BL/6J mice. Induction of MR by e-cigarettes was correlated with a reduction in 11β-HSD2 and activation of pSer9GSK3β (glycogen synthase kinase-3β phosphorylation) within the kidneys. In contrast, e-cigarettes increased the urinary ratio of corticosterone to 11-dehydrocorticosterone, reduced urinary sodium content, and elevated renal epithelial sodium channel expression. However, inhaling e-cigarettes without nicotine did not affect these metabolic parameters. Treatment with eplerenone normalized BP, reversed urinary metabolic profiles, and reduced epithelial sodium channel by inhibiting renal pSer9GSK3β in nicotine e-cigarette-exposed mice. In mouse renal CCD M1 cells, aerosol nicotine from e-cigarettes increased MR while decreasing 11β-HSD2, and these effects are likely via activation of pSer9GSK3β through a nicotinic receptor-mediated mechanism.CONCLUSIONSOur findings highlight the potential renal health damage from e-cigarettes and suggest that aerosol nicotine-mediated induction of MR action in the kidneys may contribute to electronic smoking-induced BP elevation.","PeriodicalId":13042,"journal":{"name":"Hypertension","volume":"92 1","pages":""},"PeriodicalIF":8.3,"publicationDate":"2025-07-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144594035","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":"Pulse Pressure Impairs Cognition via White Matter Disruption.","authors":"Deborah L O King, Richard N Henson, Marta Correia, James B Rowe, Cam-Can Consortium, Kamen A Tsvetanov","doi":"10.1161/HYPERTENSIONAHA.124.24543","DOIUrl":"https://doi.org/10.1161/HYPERTENSIONAHA.124.24543","url":null,"abstract":"<p><strong>Background: </strong>In older adults, elevated pulse pressure predicts cognitive decline, independent of overall blood pressure. It is proposed to compromise cerebrovascular integrity, potentially leading to brain damage, though the underlying mechanisms remain unclear. We hypothesized that pulse pressure affects cognition by disrupting white matter microstructure, and that it does so independently of other cardiovascular risk factors.</p><p><strong>Methods: </strong>Latent indices of pulse pressure, overall blood pressure, and heart rate variability were estimated in a cross-sectional, population-based cohort (n=708, aged 18-88 years). An indicator of white matter microstructure was derived from diffusion-weighted imaging, termed the peak width of skeletonized mean diffusivity (PSMD). Cognitive function was assessed using measures of processing speed.</p><p><strong>Results: </strong>In robust regression, pulse pressure was significantly associated with PSMD, with PSMD also being associated with processing speed. Thus, higher pulse pressure was associated with greater white matter disruption, which in turn was associated with slower processing. This motivated testing whether PSMD mediates the effects of pulse pressure on processing speed using structural equation models. PSMD mediated this effect, accounting for 72% of the effect after adjusting for age, and remained significant after adjusting for other cardiovascular factors. We then expanded the model to show that vascular-related changes in processing speed also drive changes in higher cognitive functions.</p><p><strong>Conclusions: </strong>High pulse pressure disrupts the microstructural integrity of white matter in the brain, leading to slower processing speed. We propose that better management of pulse pressure could help to preserve white matter integrity and reduce cognitive decline in later life.</p>","PeriodicalId":13042,"journal":{"name":"Hypertension","volume":" ","pages":""},"PeriodicalIF":6.9,"publicationDate":"2025-07-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144600244","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":"Impact of IKCa Channels on CD34+ Cells in Arteriole Remodeling in Angiotensin II-Induced Hypertension Model Mice.","authors":"Hai Tian,Xin Liao,Cheng Xie,Xiaolin Zhang,Guoqiang Ren,Pengwei Zhu,Yan Yang,Pengyun Li,Changli Liao,Chunshu Li,Qingbo Xu,Xiangyuan Pu,Jun Cheng","doi":"10.1161/hypertensionaha.124.24537","DOIUrl":"https://doi.org/10.1161/hypertensionaha.124.24537","url":null,"abstract":"BACKGROUNDMechanisms of endothelial repair in hypertension remain unclear. CD34+ cells are reported to contribute to vascular regeneration; however, their origin and regulation in hypertension are poorly understood. We investigated the role of IKCa channels in CD34+ cell-mediated endothelial repair during Ang II (angiotensin II)-induced arteriole remodeling.METHODSUsing inducible lineage tracing (Cd34-CreERT2; R26-tdTomato), we tracked nonbone marrow-derived CD34+ cells in hypertensive mice. Single-cell RNA sequencing, immunofluorescence, transwell migration assays, and patch-clamp techniques were used to analyze phenotypic transitions, ion channel activity, and signaling pathways. Bone marrow transplantation, the IKCa channel inhibitor TRAM-34, and the ERK (extracellular signal-regulated kinase) inhibitor PD98059 were used to validate functional mechanisms.RESULTSLineage tracing revealed that nonbone marrow-derived CD34+ cells contributed to endothelial repair under hypertensive conditions. Immunofluorescence analysis showed an increase in CD31+-tdTomato+ cells in the arterioles of Ang II-treated mice after 6 weeks, indicating improved endothelial integrity. Single-cell RNA sequencing revealed 2 subgroups of endothelial cells, one of which expressed stem cell markers such as CD34 (cluster of differentiation 34), Flk-1 (fetal liver kinase 1), and Sca-1 (stem cell antigen-1). Gene expression analysis showed that CD34+ cells are involved in endothelial repair through the regulation of cell migration. Importantly, IKCa channel activation facilitated CD34+ cell migration, and TRAM-34-based inhibition of IKCa channels reduced migration. Mechanistic studies revealed that Ang II enhanced CD34+ cell migration via IKCa-mediated activation of the ERK/P38 signaling pathway, promoting cytoskeletal reorganization and increased intracellular calcium levels.CONCLUSIONSArteriole-resident CD34+ cells contribute to endothelial repair in Ang II-induced hypertension. Moreover, IKCa channel upregulation facilitates CD34+ cell migration via ERK/P38 signaling, suggesting potential therapeutic targets for hypertension.","PeriodicalId":13042,"journal":{"name":"Hypertension","volume":"21 1","pages":""},"PeriodicalIF":8.3,"publicationDate":"2025-07-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144586514","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":"Systolic BP Amplification: Systematic Review and Individual Participant Meta-Analysis.","authors":"Dean S Picone,Tan V Bui,Martin G Schultz,Petr Otahal,Alun D Hughes,J Andrew Black,Berend E Westerhof,Chen-Huan Chen,Fuyou Liang,Giacomo Pucci,Hao-Min Cheng,Heath Adams,Jiguang Wang,Nathan B Dwyer,Philip Roberts-Thomson,Remi Goupil,Sarang Paleri,Scott W Eaves,Xiaoqing Peng,James E Sharman","doi":"10.1161/hypertensionaha.124.24483","DOIUrl":"https://doi.org/10.1161/hypertensionaha.124.24483","url":null,"abstract":"BACKGROUNDSystolic blood pressure (SBP) amplification is a physiological phenomenon related to the level of pressure difference between the aorta and brachial artery and is associated with cuff blood pressure (BP) measurement inaccuracy. However, knowledge on the invasively measured level of aortic-to-brachial SBP amplification is limited. This study aimed to explore this, as well as anticipated effects on hypertension classification.METHODSA systematic review and individual participant data meta-analysis identified invasive brachial and aortic BP recorded in 1151 participants (62±12 years, 72% male). SBP amplification was calculated as brachial SBP minus aortic SBP. Hypertension classification (defined according to previously described thresholds for brachial and aortic BP) was compared between the aortic and brachial BP measures.RESULTSThere was a wide range of SBP amplification, which was similar between male and female (mean±SD, 8±9 mm Hg and 7±10 mm Hg, respectively) and decreased with increasing age. High SBP amplification (>15 mm Hg) was observed in 17.4% (male, 16.8% versus female, 19.5%; P=0.44), and low SBP amplification (<5 mm Hg) in 37.3% of participants (male, 37.2% versus female, 37.4%; P=0.95). The overall level of agreement between hypertension classification based on brachial and aortic BP was moderate (κ, 0.67; P<0.001; agreement, 87.4%). Agreement in hypertension classification was 65.0%, 38.1%, and 92.7% across classifications of optimal, prehypertension, and hypertension, respectively.CONCLUSIONSIn males and females there is wide variability in aortic-to-brachial SBP amplification. There were major theoretical differences in hypertension classification based on brachial versus aortic BP. This knowledge may help toward innovations for improving cuff BP measurement accuracy.","PeriodicalId":13042,"journal":{"name":"Hypertension","volume":"47 1","pages":""},"PeriodicalIF":8.3,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144521342","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: 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}