Journal of Cardiovascular Pharmacology最新文献_第7页

The Ubiquitin Ligase HERC2 Promotes Ang II-Induced Cardiac Hypertrophy Through Destabilization of MeCP2 to Enhance Lin28a Expression. 泛素连接酶HERC2通过破坏MeCP2的稳定性来增强Lin28a的表达，从而促进血管紧张素II诱导的心肌肥大。

IF 2.6 4区医学

Journal of Cardiovascular Pharmacology Pub Date : 2025-02-01 DOI: 10.1097/FJC.0000000000001647

Bin Zhou, Hui-Fan Fu, Jiang-Feng Niu, Wei Deng, Fu-Mou Deng, Zhi-Dong Zhou, Wei Zhou, Qinggen Xiong, Chang Li

{"title":"The Ubiquitin Ligase HERC2 Promotes Ang II-Induced Cardiac Hypertrophy Through Destabilization of MeCP2 to Enhance Lin28a Expression.","authors":"Bin Zhou, Hui-Fan Fu, Jiang-Feng Niu, Wei Deng, Fu-Mou Deng, Zhi-Dong Zhou, Wei Zhou, Qinggen Xiong, Chang Li","doi":"10.1097/FJC.0000000000001647","DOIUrl":"10.1097/FJC.0000000000001647","url":null,"abstract":"Abstract: Homologous to the E6-AP carboxy terminus-type E3 ubiquitin ligases participate in the progression of cardiovascular diseases. HERC2 has been reported to play critical roles in many pathologic processes, but its role in cardiac hypertrophy remains unclear. In this study, we observed that the expression and activity of HERC2 were significantly upregulated in hypertrophic hearts and angiotensin II (Ang II)-stimulated primary cardiomyocytes. Knockdown of HERC2 in cardiomyocytes significantly alleviated the myocardial hypertrophy induced by Ang II. Conversely, cardiac-specific overexpression of HERC2 aggravated Ang II-induced cardiac hypertrophy in vitro and in vivo. Furthermore, we demonstrated that HERC2 promoted cardiac hypertrophy through increasing the expression of lin-28 homologue A (Lin28a), an RNA-binding protein that regulates pathologic cardiac hypertrophic. Knocking down Lin28a attenuated Ang II-induced myocardial hypertrophy and abolished the increase in myocardial hypertrophy by overexpression of HERC2. Further investigation indicated that HERC2 promoted the expression level of Lin28a by reducing methyl-CpG binding protein 2 (MeCP2), a transcriptional suppressor of Lin28a. We also showed that the prohypertrophic effect of HERC2 was partially dependent on MeCP2 inhibition. Mechanistically, HERC2 directly bound with MeCP2, and promotes its K48-linked polyubiquitination and degradation. Combined, these findings demonstrate that HERC2 plays a crucial role in pathologic cardiac hypertrophy, thereby indicating that targeting the HERC2/MeCP2/Lin28a axis is a potential strategy for heart failure therapy.","PeriodicalId":15212,"journal":{"name":"Journal of Cardiovascular Pharmacology","volume":" ","pages":"145-155"},"PeriodicalIF":2.6,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142583405","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}

引用次数: 0

Isorhynchophylline Inhibits Platelet Activation and Thrombus Formation. 异蛇碱抑制血小板活化和血栓形成。

IF 2.6 4区医学

Journal of Cardiovascular Pharmacology Pub Date : 2025-02-01 DOI: 10.1097/FJC.0000000000001655

Yun Liu, Hui Zhu, Yue Dai, Jie Zhang, Yingying Li, Huimin Jiang, Yueyue Sun, Jianlin Qiao, Xiaoqi Xu

{"title":"Isorhynchophylline Inhibits Platelet Activation and Thrombus Formation.","authors":"Yun Liu, Hui Zhu, Yue Dai, Jie Zhang, Yingying Li, Huimin Jiang, Yueyue Sun, Jianlin Qiao, Xiaoqi Xu","doi":"10.1097/FJC.0000000000001655","DOIUrl":"10.1097/FJC.0000000000001655","url":null,"abstract":"Abstract: Isorhynchophylline is a Chinese herbal medicine and has multiple effects such as anti-inflammatory and neuroprotective effects. Whether isorhynchophylline has antithrombotic property is unknown. This study aims to evaluate its role in platelet function. Human platelets were incubated with isorhynchophylline (0, 10, 20, and 40 μM) at 37°C for 1 hour to detect platelet aggregation and activation, receptors level, spreading, and calcium mobilization. In addition, isorhynchophylline (5 mg/kg) was injected into mice to measure in vivo hemostasis and thrombosis. Isorhynchophylline dose-dependently reduced platelet aggregation, adenosine triphosphate secretion, P-selectin expression, and α IIb β 3 activation induced by collagen-related peptide or thrombin without affecting surface level of receptors α IIb β 3 , GPIbα, and glycoprotein VI. Meanwhile, isorhynchophylline-treated platelets showed reduced spreading. Moreover, isorhynchophylline reduced platelet calcium mobilization, phosphatidylserine exposure, and the phosphorylation of PLCγ2 and PKCα. Furthermore, administration of isorhynchophylline into mice impaired platelet hemostatic function and arterial/venous thrombosis without affecting coagulation. In conclusion, isorhynchophylline impairs platelet function and arterial/venous thrombosis, implying its potential to be a novel agent for treating thrombotic or cardiovascular diseases.","PeriodicalId":15212,"journal":{"name":"Journal of Cardiovascular Pharmacology","volume":" ","pages":"137-144"},"PeriodicalIF":2.6,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142769303","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}

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Acknowledgment of Reviewers. 审稿人致谢。

IF 2.6 4区医学

Journal of Cardiovascular Pharmacology Pub Date : 2025-02-01 DOI: 10.1097/FJC.0000000000001667

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Key Genes and Biological Pathways in Pulmonary Arterial Hypertension Related to Endoplasmic Reticulum Stress Identified by Bioinformatics. 生物信息学鉴定肺动脉高压内质网应激相关的关键基因和生物学途径。

IF 2.6 4区医学

Journal of Cardiovascular Pharmacology Pub Date : 2025-02-01 DOI: 10.1097/FJC.0000000000001651

Shanzuan Wang, Debin Zhuo, Juan Lin, Chunxia Zhang

{"title":"Key Genes and Biological Pathways in Pulmonary Arterial Hypertension Related to Endoplasmic Reticulum Stress Identified by Bioinformatics.","authors":"Shanzuan Wang, Debin Zhuo, Juan Lin, Chunxia Zhang","doi":"10.1097/FJC.0000000000001651","DOIUrl":"10.1097/FJC.0000000000001651","url":null,"abstract":"Abstract: Pulmonary arterial hypertension (PAH) is a cardiopulmonary vascular condition with an unclear pathogenesis. Targeting endoplasmic reticulum (ER) stress has been suggested as a novel treatment approach for PAH, but the mechanisms involving ER stress-related genes in PAH are not well understood. Microarray data for PAH and ER stress-related genes were analyzed. Differential and Venn analyses identified 17 differentially expressed ER stress-related genes in PAH. Candidate drugs targeting these genes were predicted using the CMap database. A protein-protein interaction (PPI) network was constructed, and hub genes (LCN2, IGF1, VCAM1, EDN1, HMOX1, TLR4) with complex interplays were identified using the STRING database and Cytoscape plugins. The clinical diagnostic performance of the hub genes was evaluated using ROC curves. The GeneMANIA Web site was utilized to predict enriched pathways associated with the hub genes and their functionally similar genes. MiRNAs and transcription factors targeting the hub genes were predicted using the Networkanalyst Web site. The immune levels in control samples and PAH samples were assessed using various algorithms. Nine drug candidates were found to potentially target the identified ER stress-related genes. The hub genes and their correlated genes were significantly enriched in immune-related pathways. The PAH group showed increased immune cell infiltration, indicating a heightened immune response. This study sheds light on the role of ER stress-associated hub genes in PAH and proposes potential drugs targeting these genes. These findings provide valuable insights into PAH mechanisms and support the exploration of ER stress as a therapeutic target.","PeriodicalId":15212,"journal":{"name":"Journal of Cardiovascular Pharmacology","volume":"85 2","pages":"108-119"},"PeriodicalIF":2.6,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143188860","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}

引用次数: 0

Impact of Boldine Treatment on Hypertrophy and Lipid Peroxidation in the Right Ventricle Subjected to Experimental Adrenergic Overstimulation. 波定治疗对实验性肾上腺素能过度刺激右心室肥厚和脂质过氧化的影响。

IF 2.6 4区医学

Journal of Cardiovascular Pharmacology Pub Date : 2025-02-01 DOI: 10.1097/FJC.0000000000001657

Elissa Kerli Fernandes, Patrick Türck, Cristina Campos Carraro, Victor de Mello Palma, Gabriel de Lima Rosa, Adriana Simon Coitinho, Fernanda Visioli, Adriane Belló-Klein, Alexandre Luz de Castro, Alex Sander da Rosa Araujo

{"title":"Impact of Boldine Treatment on Hypertrophy and Lipid Peroxidation in the Right Ventricle Subjected to Experimental Adrenergic Overstimulation.","authors":"Elissa Kerli Fernandes, Patrick Türck, Cristina Campos Carraro, Victor de Mello Palma, Gabriel de Lima Rosa, Adriana Simon Coitinho, Fernanda Visioli, Adriane Belló-Klein, Alexandre Luz de Castro, Alex Sander da Rosa Araujo","doi":"10.1097/FJC.0000000000001657","DOIUrl":"10.1097/FJC.0000000000001657","url":null,"abstract":"Abstract: Adrenergic overstimulation is detrimental to the left ventricle. However, its effects on the right ventricle (RV) are not clear. Because adrenergic overload increases metabolic demand and oxidative stress, boldine could be a therapeutic option in the treatment of cardiovascular disease because of its antioxidant role. This study aimed to investigate the impact of adrenergic overload on RV remodeling and the cardioprotective effect of boldine. Animals were divided into 4 groups: control (C), boldine (25 mg/kg i. P .) (B), isoproterenol (ISO) (5 mg/kg subcutaneously), and boldine+isoproterenol (B+ISO). Echocardiography, Fulton index (FI), histology, oxidative stress, inflammation, and β-adrenergic receptor (ADR) were analyzed. The diastolic parasternal length [C 0.698 (0.623-0.724) versus ISO 0.77 (0.73-0.81)], FI [C 0.268 (0.231-0.275) versus ISO 0.340 (0.280-0.353)], inflammatory infiltration (∼40%), and ADR [C 0.78 (0.71-0.84) versus ISO 1.74 (1.52-2.00)] were increased in the ISO group ( P < 0.05). Boldine treatment (B+ISO) reduced the FI [0.240 (0.228-0.263)], lipid peroxidation [2.07 (2.01-2.61)], and ADR [0.71(0.62-0.80)]. Boldine increased total SH levels in B+ISO [C 2.4 (1.78-2.71); ISO 4.01 (2.95-4.66) versus B+ISO 6.77(5.15-8.60)] ( P < 0.05). There was a positive correlation between lipid peroxidation and the FI, and a negative correlation between total SH and the FI ( P < 0.05). This is the first study to explore the effects of adrenergic overstimulation on RV and the protective effect of boldine. Such data pave the way for further research involving RV remodeling, such as in pulmonary hypertension, and a new therapeutic option.","PeriodicalId":15212,"journal":{"name":"Journal of Cardiovascular Pharmacology","volume":" ","pages":"166-175"},"PeriodicalIF":2.6,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142785855","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}

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Correlation of Hyaluronic Acid (HA), Syndecan-1 (SDC-1), Heparan Sulfate (HS) With Early Stage End Organ Dysfunction in Sepsis Patients. 透明质酸（HA）、Syndecan-1 （SDC-1）、硫酸肝素（HS）与脓毒症患者早期及器官功能障碍的相关性

IF 2.6 4区医学

Journal of Cardiovascular Pharmacology Pub Date : 2025-02-01 DOI: 10.1097/FJC.0000000000001654

Zhengchao Li, Xingpeng Jiang, Jinghui Li, Yuzhu Wang

{"title":"Correlation of Hyaluronic Acid (HA), Syndecan-1 (SDC-1), Heparan Sulfate (HS) With Early Stage End Organ Dysfunction in Sepsis Patients.","authors":"Zhengchao Li, Xingpeng Jiang, Jinghui Li, Yuzhu Wang","doi":"10.1097/FJC.0000000000001654","DOIUrl":"10.1097/FJC.0000000000001654","url":null,"abstract":"Abstract: The aim of this study was to explore the relationship between the changes in early degradation products of polysaccharide coatings [such as hyaluronic acid (HA), syndecan-1 (SDC-1), and heparan sulfate (HS)] and the development of organ dysfunction in sepsis patients. We conducted a retrospective analysis on 140 sepsis patients admitted from January 2021 to June 2022, who formed the study group; 100 healthy individuals who underwent health checks during the same period were included as the control group. The study found that the expression levels of HA, SDC-1, and HS on admission and within 24 hours of admission in sepsis patients, as well as the early change rates, were positively correlated with organ dysfunction ( P < 0.05). Through receiver operating characteristic curve analysis, we discovered that the early change rates of HA, SDC-1, and HS have high predictive value for organ dysfunction in sepsis patients, with the combined predictive value being the most significant. The study conclusion points out that the increased levels of HA, SDC-1, HS, and other degradation products of polysaccharide coatings in the early stage of sepsis are positively associated with the occurrence of organ dysfunction. Clinicians can use the early expression changes of these biomarkers to predict the risk of organ dysfunction in sepsis patients, enabling timely implementation of preventive measures that may improve patient outcomes.","PeriodicalId":15212,"journal":{"name":"Journal of Cardiovascular Pharmacology","volume":" ","pages":"129-136"},"PeriodicalIF":2.6,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143005952","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}

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The Research Progress: Cuproptosis and Copper Metabolism in Regulating Cardiovascular Diseases. 研究进展：调节心血管疾病的铜氧化酶和铜代谢。

IF 2.6 4区医学

Journal of Cardiovascular Pharmacology Pub Date : 2025-02-01 DOI: 10.1097/FJC.0000000000001653

Liu Yanjuan, Deng Shuangyou, Wang Ying, Chen Xing, Chen Yue, Yu Zixuan, Zhang Shumeng, Chen Lingli, Li Jie

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Melatonin Attenuates Cardiac Dysfunction and Inflammation in Dilated Cardiomyopathy via M2 Macrophage Polarization. 褪黑素通过M2巨噬细胞极化减轻扩张型心肌病的心脏功能障碍和炎症反应

IF 2.6 4区医学

Journal of Cardiovascular Pharmacology Pub Date : 2025-02-01 DOI: 10.1097/FJC.0000000000001650

Bin Qi, Qing-Feng Wu, Zhi-Jie Yang, Nan Huang, Liu Miao

{"title":"Melatonin Attenuates Cardiac Dysfunction and Inflammation in Dilated Cardiomyopathy via M2 Macrophage Polarization.","authors":"Bin Qi, Qing-Feng Wu, Zhi-Jie Yang, Nan Huang, Liu Miao","doi":"10.1097/FJC.0000000000001650","DOIUrl":"10.1097/FJC.0000000000001650","url":null,"abstract":"Abstract: Melatonin is a neuroendocrine hormone that exerts protective effects on the heart. Increasing evidence suggests that macrophage M2-type polarization improves myocardial regeneration and repair. Therefore, this study investigated whether melatonin ameliorates dilated cardiomyopathy (DCM) by modulating M2-type polarization. DCM mice were established by induction with doxorubicin and then treated with melatonin. Cardiac dysfunction was determined by measuring left ventricular ejection fraction and left ventricular internal dimensions at end-diastole and end-systole. Heart injury and fibrosis were determined by hematoxylin and eosin staining and Sirius Red staining, respectively. Serum concentrations of melatonin, tumor necrosis factor-alpha (TNF-α), interleukin-1 beta (IL-1β), and interleukin-6 (IL-6) were measured through enzyme-linked immunosorbent assays. M2-type macrophages were analyzed by flow cytometry. Relative mRNA and protein levels were determined by reverse transcription quantitative polymerase chain reaction and Western blotting, respectively. Circulating melatonin levels were significantly decreased in DCM mice and were associated with left ventricular ejection fraction. Treatment with melatonin markedly ameliorated cardiac dysfunction, improved survival, and alleviated pathologic changes and collagen deposition in DCM mice. Furthermore, melatonin-treated DCM mice displayed lower serum and cardiac levels of IL-1β, IL-6, and TNF-α, as well as higher number of M2-type macrophages in cardiac tissue, indicating that melatonin treatment could decrease inflammatory responses and facilitate M2 macrophage polarization in DCM mice. Thus, melatonin treatment alleviated cardiac dysfunction and inflammatory responses by promoting M2 macrophage polarization in the DCM mouse model.","PeriodicalId":15212,"journal":{"name":"Journal of Cardiovascular Pharmacology","volume":" ","pages":"156-165"},"PeriodicalIF":2.6,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142621335","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}

引用次数: 0

Changes for 2025 at Journal of Cardiovascular Pharmacology: Introducing Our Junior Associate Editors, Podcasts, Feature, and New Board Members. 心血管药理学杂志2025年的变化：介绍我们的初级副编辑，播客，特写和新的董事会成员。

IF 2.6 4区医学

Journal of Cardiovascular Pharmacology Pub Date : 2025-01-21 DOI: 10.1097/FJC.0000000000001673

Antonio Abbate, Giuseppe Biondi-Zoccai, Raffaele Altara, George W Booz

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Investigating the Transfer of Lisinopril Into Human Milk: A Quantitative Analysis. 利辛普利向母乳转移的研究：定量分析

IF 2.6 4区医学

Journal of Cardiovascular Pharmacology Pub Date : 2025-01-01 DOI: 10.1097/FJC.0000000000001642

Julie Chugh, Jean Dai, Palika Datta, Kaytlin Krutsch

{"title":"Investigating the Transfer of Lisinopril Into Human Milk: A Quantitative Analysis.","authors":"Julie Chugh, Jean Dai, Palika Datta, Kaytlin Krutsch","doi":"10.1097/FJC.0000000000001642","DOIUrl":"10.1097/FJC.0000000000001642","url":null,"abstract":"Abstract: Lisinopril is commonly prescribed to manage conditions such as hypertension and heart failure. Although concerns about fetal toxicity have traditionally limited the use of lisinopril in women of reproductive age, recent American College of Obstetricians and Gynecologists guidelines promote aggressive treatment of hypertension, which may require the use of pharmacologic agents not previously considered in the postpartum period. We aimed to estimate infant exposure to maternal lisinopril through breast milk and report the tolerance of the breastfed infant. Five volunteers taking lisinopril provided samples of their human milk and their associated health information for research through the InfantRisk Center Human Milk Biorepository. The milk pharmacokinetics of lisinopril were measured using liquid chromatography-mass spectrometry. The mean milk concentration of lisinopril was 0.49 ng/mL per 10 mg daily dose. The relative infant dose was 0.06% for lisinopril, more than 100 times lower than the standard 10% safety threshold. The minimal transfer of lisinopril into human milk in this study suggests the drug is unlikely to pose a clinically significant risk to healthy breastfed infants.","PeriodicalId":15212,"journal":{"name":"Journal of Cardiovascular Pharmacology","volume":" ","pages":"84-87"},"PeriodicalIF":2.6,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142466353","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}

引用次数: 0