Journal of Cardiovascular Pharmacology最新文献_第4页

High Dose of Liraglutide Impairs Renal Function in Female Hypertensive Rats. 大剂量利拉鲁肽会损害雌性高血压大鼠的肾功能

IF 2.6 4区医学

Journal of Cardiovascular Pharmacology Pub Date : 2025-02-01 DOI: 10.1097/FJC.0000000000001649

Felipe Tonon Firmino, Pollyana Peixoto, Thatiany Jardim Batista, Leonardo da Silva Escouto, Girlandia Alexandre Brasil, Mariana Dos Reis Couto, Antonio Ferreira de Melo Júnior, Nazaré Souza Bissoli

{"title":"High Dose of Liraglutide Impairs Renal Function in Female Hypertensive Rats.","authors":"Felipe Tonon Firmino, Pollyana Peixoto, Thatiany Jardim Batista, Leonardo da Silva Escouto, Girlandia Alexandre Brasil, Mariana Dos Reis Couto, Antonio Ferreira de Melo Júnior, Nazaré Souza Bissoli","doi":"10.1097/FJC.0000000000001649","DOIUrl":"10.1097/FJC.0000000000001649","url":null,"abstract":"Abstract: Glucagon-like peptide-1 receptor agonists exhibit beneficial cardiovascular effects. However, the renal effects of different doses of liraglutide in an essential hypertension model have not yet been investigated. Female spontaneously hypertensive rats were treated for 30 days, twice a day, with saline (control) or liraglutide at low (0.06 mg/kg) and high (LH, 0.6 mg/kg) doses. Volume intake and excretion were monitored for a period of 24 hours. In renal tissue, nitrite, nitrate, advanced protein oxidation products, collagen deposition, creatinine (Cr), urea (U), sodium, and potassium were analyzed. Liraglutide reduced body weight gain in both groups. However, in the high dose, it increased urinary volume excretion and sodium/potassium ratio. Both doses reduced the urinary U/Cr ratio and LH increased the serum U/Cr ratio. Advanced protein oxidation products were reduced only in low liraglutide. LH augmented collagen and early markers of kidney injury (blood urea nitrogen, blood urea nitrogen/Cr). LH increased nitrate, reduced nitrite, and caused an aberrant increase in glomerular filtration rate. Both doses' effects were independent of blood pressure and glycemic control. Liraglutide appears to have distinct effects on the hypertensive female kidney depending on the dose, with higher doses impairing kidney function.","PeriodicalId":15212,"journal":{"name":"Journal of Cardiovascular Pharmacology","volume":" ","pages":"120-128"},"PeriodicalIF":2.6,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142604911","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

A Decadal Exploration of Cutaneous Adverse Effects of FDA-Approved Cardiovascular Medications: Insights From 2013 to 2023. fda批准的心血管药物皮肤不良反应的十年探索：2013年至2023年的见解。

IF 2.6 4区医学

Journal of Cardiovascular Pharmacology Pub Date : 2025-02-01 DOI: 10.1097/FJC.0000000000001660

Anika Jallorina, Kunal Vij, Leo Wan, Joson Thomas, David Drum, Sharon A Glick, Mary F Lee-Wong

{"title":"A Decadal Exploration of Cutaneous Adverse Effects of FDA-Approved Cardiovascular Medications: Insights From 2013 to 2023.","authors":"Anika Jallorina, Kunal Vij, Leo Wan, Joson Thomas, David Drum, Sharon A Glick, Mary F Lee-Wong","doi":"10.1097/FJC.0000000000001660","DOIUrl":"10.1097/FJC.0000000000001660","url":null,"abstract":"Abstract: Given the high prevalence of cardiovascular disease in the United States, there is a critical need for new medications to improve the outcomes of these diseases. The US Food and Drug Administration has approved numerous medications that are able to effectively do so. While these drugs have significantly beneficial effects, just like any other medication, they can come with a multitude of unwanted side effects. It has been noted that cardiovascular drugs have been associated with a considerable number of dermatologic reactions. This review examines current literature on the various cutaneous manifestations of these adverse reactions. It focuses on these newly Food and Drug Administration-approved cardiovascular medications from 2013 to 2023, detailing both common and rare effects in the past decade. As more medications continue to enter the market, the necessity for awareness of more systemic side effects will continue to grow. This comprehensive review aims to guide clinicians in identifying drug-induced reactions in patients on these therapies.","PeriodicalId":15212,"journal":{"name":"Journal of Cardiovascular Pharmacology","volume":" ","pages":"97-107"},"PeriodicalIF":2.6,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142785851","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

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}

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}

引用次数: 0

Acknowledgment of Reviewers.

IF 2.6 4区医学

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

引用次数: 0

Key Genes and Biological Pathways in Pulmonary Arterial Hypertension Related to Endoplasmic Reticulum Stress Identified by Bioinformatics.

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":"https://doi.org/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

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}

引用次数: 0

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

引用次数: 0

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