Clinical and Experimental Hypertension最新文献

{"title":"FGF21 attenuates salt-sensitive hypertension via regulating HNF4α/ACE2 axis in the hypothalamic paraventricular nucleus of mice.","authors":"Wei Xu, Xia Gao, Hao Luo, Yingmei Chen","doi":"10.1080/10641963.2024.2361671","DOIUrl":"10.1080/10641963.2024.2361671","url":null,"abstract":"<p><strong>Background: </strong>Fibroblast growth factor 21 (FGF21) has a protective effect against cardiovascular disease. However, the role of FGF21 in hypertension remains elusive.</p><p><strong>Methods: </strong>Ten-week-old male C57BL/6 mice were randomly divided into normal-salt (NS) group, NS+FGF21 group, deoxycorticosterone acetate-salt (DOCA) group and DOCA+FGF21 group. The mice in NS group underwent uninephrectomy without receiving DOCA and 1% NaCl and the mice in DOCA group were subjected to uninephrectomy and DOCA-salt (DOCA and 1% NaCl) treatment for 6 weeks. At the same time, the mice were infused with vehicle (artificial cerebrospinal fluid, aCSF) or FGF21 (1 mg/kg) into the bilateral paraventricular nucleus (PVN) of mice.</p><p><strong>Results: </strong>Here, we showed that FGF21 treatment lowered DOCA salt-induced inflammation and oxidative stress in the PVN, which reduced sympathetic nerve activity and hypertension. Mechanistically, FGF21 treatment decreased the expression of HNF4α and inhibited the binding activity of HNF4α to the promoter region of ACE2 in the PVN of DOCA salt-treated mice, which further up-regulated ACE2/Ang (1-7) signals in the PVN. In addition, ACE2 deficiency abolished the protective effect of FGF21 in DOCA salt-treated mice, suggesting that FGF21-mediated antihypertensive effect was dependent on ACE2.</p><p><strong>Conclusions: </strong>The results demonstrate that FGF21 protects against salt-sensitive hypertension via regulating HNF4α/ACE2/Ang (1-7) axis in the PVN of DOCA salt-treated mice via multi-organ crosstalk between liver, brain and blood vessels.</p>","PeriodicalId":10333,"journal":{"name":"Clinical and Experimental Hypertension","volume":"46 1","pages":"2361671"},"PeriodicalIF":12.3,"publicationDate":"2024-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141260906","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Omentin-1 ameliorates pulmonary arterial hypertension by inhibiting endoplasmic reticulum stress through AMPKα signaling.","authors":"Xinyu Deng, Hao Luo, Jing He, Wang Deng, Daoxin Wang","doi":"10.1080/10641963.2024.2332695","DOIUrl":"10.1080/10641963.2024.2332695","url":null,"abstract":"<p><strong>Background: </strong>Endothelial dysfunction of the pulmonary artery contributes to hypoxia-induced pulmonary arterial hypertension (PAH). Omentin-1, as a novel adipocytokine, plays an important protective role against cardiovascular diseases. However, the effect and underlying mechanisms of omentin-1 against PAH remain unclear.</p><p><strong>Methods: </strong>PAH was induced in SD (Sprague & Dawley) rats via a low-oxygen chamber for 4 weeks. Hemodynamic evaluation was undertaken using a PowerLab data acquisition system, and histopathological analysis was stained with hematoxylin and eosin (H&E). Endothelial function of pulmonary artery was assessed using wire myography.</p><p><strong>Results: </strong>We found that omentin-1 significantly improved pulmonary endothelial function in rats exposed to hypoxia and attenuated PAH. Mechanistically, we found that omentin-1 increased phosphorylated 5'‑adenosine monophosphate‑activated protein kinase (p‑AMPK) level and reduced endoplasmic reticulum (ER) stress and increased NO production in pulmonary artery from rats exposed to hypoxia. However, the effect of omentin-1 was abolished by treatment with AMPK inhibitor (Compound C).</p><p><strong>Conclusions: </strong>Our results reveal a protective effect of omentin-1 in PAH via inhibiting ER stress through AMPKα signaling and provide an agent with translational potential for the treatment of PAH.</p>","PeriodicalId":10333,"journal":{"name":"Clinical and Experimental Hypertension","volume":"46 1","pages":"2332695"},"PeriodicalIF":12.3,"publicationDate":"2024-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140287121","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The proliferation/migration ability mediated by CD151/PI3K/AKT pathway determines the therapeutic effect of hUC-MSCs transplantation on rheumatoid arthritis.","authors":"Xuewei Xia, Peixin Shen, Guomei Yang, Mengwei Yao, Xiaofeng Wu, Lina Lyu, Yanji He, Zhuxin Li, Wei Wang, Yi Yang, Xiang Ao, Chuanjiang Xia, Zhuo Chen, Xiang Xu","doi":"10.1080/10641963.2024.2366270","DOIUrl":"https://doi.org/10.1080/10641963.2024.2366270","url":null,"abstract":"<p><strong>Objective: </strong>To elucidate the underlying mechanism by which the proliferation and migration abilities of human umbilical cord mesenchymal stem cells (hUC-MSCs) determine their therapeutic efficacy in rheumatoid arthritis treatment.</p><p><strong>Methods: </strong>The DBA/1J mice were utilized to establish a collagen-induced RA (CIA) mouse model and to validate the therapeutic efficacy of hUC-MSCs transfected with CD151 siRNA. RNA-seq, QT-PCR and western blotting were utilized to evaluate the mRNA and protein levels of the PI3K/AKT pathway, respectively.</p><p><strong>Results: </strong>IFN-γ significantly enhanced the proliferation and migration abilities of hUC-MSCs, up-regulating the expression of CD151, a gene related to cell proliferation and migration. Effective inhibition of this effect was achieved through CD151 siRNA treatment. However, IFN-γ did not affect hUC-MSCs differentiation or changes in cell surface markers. Additionally, transplantation of CD151-interfered hUC-MSCs (siRNA-CD151-hUC-MSCs) resulted in decreased colonization in the toes of CIA mice and worse therapeutic effects compared to empty vector treatment (siRNA-NC-hUC-MSCs).</p><p><strong>Conclusion: </strong>IFN-γ facilitates the proliferation and migration of hUC-MSCs through the CD151/PI3K/AKT pathway. The therapeutic efficacy of siRNA-CD151-hUC-MSCs was found to be inferior to that of siRNA-NC-hUC-MSCs.</p>","PeriodicalId":10333,"journal":{"name":"Clinical and Experimental Hypertension","volume":"46 1","pages":"2366270"},"PeriodicalIF":12.3,"publicationDate":"2024-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141305581","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Gestational diabetes causes hyperactivity of the sympathetic nervous system and hypertension in adult mice offspring.","authors":"Li Yang, Xingyu Zhu, Jun Zhu, Zegang Hu, Chunxiang Wang, Hao Luo, Xue Bai","doi":"10.1080/10641963.2024.2402260","DOIUrl":"https://doi.org/10.1080/10641963.2024.2402260","url":null,"abstract":"<p><strong>Background: </strong>Gestational diabetes can lead to increased blood pressure in offspring, accompanied by impaired renal sodium excretion function and vasoconstriction and diastole dysfunction. However, there are few studies on whether it is accompanied by increased sympathetic nerve activity.</p><p><strong>Methods: </strong>Pregnant C57BL/6 mice were intraperitoneally injected with streptozotocin (35 mg/kg) or citrate buffer at day 0 of gestation. The mice of control mother offspring (CMO) and diabetic mother offspring (DMO) at 16 weeks of age were infused with vehicle (artificial cerebrospinal fluid, aCSF, 0.4 μL/h) or tempol (1 mmol/L, 0.4 μL/h) into the bilateral paraventricular nucleus (PVN) of mice for 4 weeks, respectively.</p><p><strong>Results: </strong>Compared with CMO group, SBP and peripheral sympathetic nerve activity (increased heart rate, LF/HF and plasma norepinephrine and decreased SDNN and RMSSD) were increased in DMO group, which was accompanied by increased angiotensin II type-1 receptor (AT₁R) expression and function in PVN. The increase in AT₁R expression levels was attributed to a decrease in the methylation level of the AT₁R promoter region, resulting in an increase in AT₁R mRNA levels in PVN of DMO. Moreover, compared with CMO group, the levels of oxidative stress were increased and DNMT1 expression was decreased in PVN of DMO. Bilateral PVN infusion of tempol attenuated oxidative stress increased the level of DNMT1 expression and the binding of DNMT1 to the AT₁R promoter region, which reduced mRNA and protein expression level of AT₁R, heart rate and SBP in DMO, but not in CMO.</p><p><strong>Conclusions: </strong>The present study provides evidence for overactive sympathetic nervous systems in the pathogenesis of gestational diabetes-induced hypertension in offspring. Central antioxidant intervention in the PVN may be an important treatment strategy for fetal-programmed hypertension.</p>","PeriodicalId":10333,"journal":{"name":"Clinical and Experimental Hypertension","volume":"46 1","pages":"2402260"},"PeriodicalIF":1.5,"publicationDate":"2024-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142281293","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The association of schooling, sibling life situation, and dietary habits with the estimated 24-h urinary salt excretion and sodium-to-potassium ratio in 3-year-old children.","authors":"Kiyoko Odani, Kengo Yoshii, Natsuki Maruyama, Sayumi Takahata, Sadahiro Kawazoe, Takashi Miyawaki, Akane Higashi","doi":"10.1080/10641963.2024.2421003","DOIUrl":"https://doi.org/10.1080/10641963.2024.2421003","url":null,"abstract":"<p><strong>Objectives: </strong>We examined the association of schooling, sibling life situation, and dietary habits with the estimated 24-h urinary salt excretion and the urinary sodium-to-potassium (Na/K) ratio in 3-year-old children.</p><p><strong>Methods: </strong>The subjects were 639 children who underwent a health checkup in four cities and towns in Kyoto Prefecture from January to November 2019. The children's parents answered questionnaires about weekday childcare places, the birth order, and the awareness of reducing the salt intake. The questions on food intake frequency included 10 items. The estimated 24-h salt excretion and Na/K ratio were calculated from the participants' first voiding urine in the morning.</p><p><strong>Results: </strong>Data were available for 294 children. The median (interquartile range (IQR)) of salt excretion (g/day) was 2.6 (1.7-3.4), and urinary Na/K ratio (mmol ratio) was 2.6 (1.6-4.1). Multinomial logistic regression analysis showed that the group with older siblings was significantly associated with high salt (odds ratio 1.89 (95% confidence interval 1.04 to 3.46)). In the urinary Na/K ratio, the nursery group had a significantly lower Na/K (odds ratio 0.32 (0.17 to 0.60)). High processed meat products intake was associated with a higher Na/K (odds ratio 1.96 (1.05-3.66)), whereas high vegetable intake was associated with a lower Na/K (odds ratio 0.45 (0.23-0.87)). Other factors showed no significant associations.</p><p><strong>Conclusions: </strong>In Japanese 3-year-old children, the estimated 24-h urinary salt excretion was associated with older siblings, and the urinary Na/K ratios were associated with schooling situation and the intake of processed meat products and vegetables.</p>","PeriodicalId":10333,"journal":{"name":"Clinical and Experimental Hypertension","volume":"46 1","pages":"2421003"},"PeriodicalIF":1.5,"publicationDate":"2024-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142521187","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Inhibition of DYRK1A attenuates vascular remodeling in pulmonary arterial hypertension via suppressing STAT3/Pim-1/NFAT pathway.","authors":"Cong Lan, Guangyao Fang, Chenming Qiu, Xiuchuan Li, Fengyuan Yang, Yongjian Yang","doi":"10.1080/10641963.2023.2297642","DOIUrl":"10.1080/10641963.2023.2297642","url":null,"abstract":"<p><p>Pulmonary arterial hypertension (PAH) is characterized by progressive vascular remodeling caused by the excessive proliferation and survival of pulmonary artery smooth muscle cells (PASMCs). Dual-specificity tyrosine regulated kinase 1A (DYRK1A) is a pleiotropic kinase involved in the regulation of multiple biological functions, including cell proliferation and survival. However, the role and underlying mechanisms of DYRK1A in PAH pathogenesis remain unclear. We found that DYRK1A was upregulated in PASMCs in response to hypoxia, both <i>in vivo</i> and <i>in vitro</i>. Inhibition of DYRK1A by harmine significantly attenuated hypoxia-induced pulmonary hypertension and pulmonary artery remodeling. Mechanistically, we found that DYRK1A promoted pulmonary arterial remodeling by enhancing the proliferation and survival of PASMCs through activating the STAT3/Pim-1/NFAT pathway, because STAT3 gain-of-function via adeno-associated virus serotype 2 (AAV2) carrying the constitutively active form of STAT3 (STAT3C) nearly abolished the protective effect of harmine on PAH. Collectively, our results reveal a significant role for DYRK1A in pulmonary arterial remodeling and suggest it as a drug target with translational potential for the treatment of PAH.</p>","PeriodicalId":10333,"journal":{"name":"Clinical and Experimental Hypertension","volume":"46 1","pages":"2297642"},"PeriodicalIF":12.3,"publicationDate":"2024-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139039598","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Association between the triglyceride-glucose index and carotid artery plaque burden in patients with primary hypertension: A cross-sectional study.","authors":"Shanshan Liu, Hao Zhang, Miao Wu, Zhixian Zhou, Yao Xiao, Qiang Wan, Zhihui Lan, Chao Rong","doi":"10.1080/10641963.2024.2383232","DOIUrl":"https://doi.org/10.1080/10641963.2024.2383232","url":null,"abstract":"<p><strong>Background: </strong>Studies have shown an association between the triglyceride-glucose (TyG) index and carotid artery plaque (CAP). However, the relationship between the TyG index and plaque burden in individuals with primary hypertension remains uncertain. Our study specifically aimed to explore this relationship among primary hypertension patients.</p><p><strong>Methods: </strong>This study involved 5,153 hospitalized patients diagnosed with primary hypertension who were undergoing treatment at the Affiliated Hospital of Jiangxi University of Chinese Medicine. We utilized multivariate logistic regression, penalized spline regression, and generalized additive models to assess the association between the TyG index and CAP burden.</p><p><strong>Results: </strong>There were 2,400 patients with primary hypertension in all. The multivariate study, which took into account all covariables, showed a positive correlation between the TyG index and CAP (OR: 1.25, 95% CI: 1.04-1.5). When the TyG index was evaluated as quartiles, the risk of CAP in the Q3 and Q4 levels of the TyG index were 1.4 (95% CI: 1.03-1.91) and 1.54 (95% CI: 1.11-2.14) times greater than in the Q1 level after adjusting for all covariables (<i>P</i> for trend < .05). Regardless of whether the TyG index was used as a continuous variable or a categorical variable, it has no significant association with the risk of single plaque after adjusting for all confounders (<i>p</i> ≥ .05). The TyG index was found to be substantially correlated with the presence of multiple plaques when analyzed as a continuous variable (OR: 1.32, 95% CI: 1.09-1.59, <i>p</i> = .004). When the TyG index was evaluated as quartiles, the adjusted OR in Q3 and Q4 were 1.49 (95% CI: 1.06-2.1) and 1.67 (95% CI: 1.16-2.41), respectively, with Q1 as reference (<i>P</i> for trend = .005). The relationship between the TyG index and the presence of multiple plaques is also consistent in all subgroups.</p><p><strong>Conclusion: </strong>The TyG index is positively associated with the presence of multiple plaques in patients with primary hypertension, whereas no association is found between the TyG index and the presence of a single carotid plaque.</p>","PeriodicalId":10333,"journal":{"name":"Clinical and Experimental Hypertension","volume":"46 1","pages":"2383232"},"PeriodicalIF":1.5,"publicationDate":"2024-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141751264","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Irisin mitigates salt-sensitive hypertension via regulating renal AMPK-Rac1 pathway.","authors":"Jie Mao, Xiaocui Zhang, Chunxiang Wang, Suying Peng","doi":"10.1080/10641963.2024.2402258","DOIUrl":"https://doi.org/10.1080/10641963.2024.2402258","url":null,"abstract":"<p><strong>Background: </strong>Irisin, as a myokine, plays a protective role against cardiovascular disease, including myocardial infarction, atherosclerosis and hypertension. However, whether irisin attenuates salt-sensitive hypertension and the related underlying mechanisms is unknown.</p><p><strong>Methods: </strong>Male Dahl salt-resistant (DSR) and Dahl salt-sensitive (DSS) (12 weeks) rats were fed a high salt diet (8% NaCl) with or without irisin treatment by intraperitoneal injection for 8 weeks.</p><p><strong>Results: </strong>Compared with DSR rats, DSS rats showed higher systolic blood pressure (SBP), impaired natriuresis and diuresis and renal dysfunction. In addition, it was accompanied by downregulation of renal p-AMPKα and upregulation of renal RAC1 and nuclear mineralocorticoid receptor (MR). Irisin intervention could significantly up-regulated renal p-AMPKα level and down-regulated renal RAC1-MR signal, thereby improving renal sodium excretion and renal function, and ultimately reducing blood pressure in DSS rats. <i>Ex vivo</i> treatment with irisin reduced the expression of RAC1 and nuclear MR in primary renal distal convoluted tubule cells from DSS rats and the effects of irisin were abolished by cotreatment of compound C (AMPK inhibitor), indicating that the regulation of RAC1-MR signals by irisin depended on the activation of AMPK.</p><p><strong>Conclusions: </strong>Irisin administration lowered salt-sensitive hypertension through regulating RAC1-MR signaling via activation of AMPK, which may be a promising therapeutic approach for salt-sensitive hypertension.</p>","PeriodicalId":10333,"journal":{"name":"Clinical and Experimental Hypertension","volume":"46 1","pages":"2402258"},"PeriodicalIF":1.5,"publicationDate":"2024-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142281294","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A smartwatch sphygmomanometer-based model for predicting short-term new-onset hypertension in individuals with high-normal blood pressure: a cohort study.","authors":"Yuqi Liu, Zhonghua Lv, Shanshan Zhou, Zihao Fu, Yifei Wang, Li Yi, Xiaolong Li, Ying Wang, Shunying Hu, Zhirui Zhou, Yundai Chen","doi":"10.1080/10641963.2024.2304023","DOIUrl":"10.1080/10641963.2024.2304023","url":null,"abstract":"<p><strong>Objectives: </strong>The objective was to utilize a smartwatch sphygmomanometer to predict new-onset hypertension within a short-term follow-up among individuals with high-normal blood pressure (HNBP).</p><p><strong>Methods: </strong>This study consisted of 3180 participants in the training set and 1000 participants in the validation set. Participants underwent both ambulatory blood pressure monitoring (ABPM) and home blood pressure monitoring (HBPM) using a smartwatch sphygmomanometer. Multivariable Cox regressions were used to analyze cumulative events. A nomogram was constructed to predict new-onset hypertension. Discrimination and calibration were assessed using the C-index and calibration curve, respectively.</p><p><strong>Results: </strong>Among the 3180 individuals with HNBP in the training set, 693 (21.8%) developed new-onset hypertension within a 6-month period. The nomogram for predicting new-onset hypertension had a C-index of 0.854 (95% CI, 0.843-0.867). The calibration curve demonstrated good agreement between the nomogram's predicted probabilities and actual observations for short-term new-onset hypertension. In the validate dataset, during the 6-month follow-up, the nomogram had a good C-index of 0.917 (95% CI, 0.904-0.930) and a good calibration curve. As the score increased, the risk of new-onset hypertension significantly increased, with an HR of 8.415 (95% CI: 5.153-13.744, <i>p</i> = .000) for the middle-score vs. low-score groups and 86.824 (95% CI: 55.071-136.885, <i>p</i> = .000) for the high-score vs. low-score group.</p><p><strong>Conclusions: </strong>This study provides evidence for the use of smartwatch sphygmomanometer to monitor blood pressure in individuals at high risk of developing new-onset hypertension in the near future.</p><p><strong>Trial registration: </strong>ChiCTR2200057354.</p>","PeriodicalId":10333,"journal":{"name":"Clinical and Experimental Hypertension","volume":"46 1","pages":"2304023"},"PeriodicalIF":12.3,"publicationDate":"2024-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139721875","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correction.","authors":"","doi":"10.1080/10641963.2024.2434292","DOIUrl":"https://doi.org/10.1080/10641963.2024.2434292","url":null,"abstract":"","PeriodicalId":10333,"journal":{"name":"Clinical and Experimental Hypertension","volume":"46 1","pages":"2434292"},"PeriodicalIF":1.5,"publicationDate":"2024-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142799441","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}