Subjects -> MEDICAL SCIENCES (Total: 8665 journals)
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CARDIOVASCULAR DISEASES (338 journals)            First | 1 2     

Showing 201 - 338 of 338 Journals sorted alphabetically
JMIR Cardio     Open Access  
Jornal Vascular Brasileiro     Open Access  
Journal of Clinical & Experimental Cardiology     Open Access   (Followers: 5)
Journal of Arrhythmia     Open Access  
Journal of Cardiac Critical Care TSS     Open Access   (Followers: 2)
Journal of Cardiac Failure     Hybrid Journal   (Followers: 1)
Journal of Cardio-Thoracic Medicine     Open Access   (Followers: 3)
Journal of Cardiobiology     Open Access  
Journal of Cardiology     Full-text available via subscription   (Followers: 7)
Journal of Cardiology and Cardiovascular Medicine     Open Access   (Followers: 3)
Journal of Cardiology and Therapy     Open Access   (Followers: 2)
Journal of Cardiology Cases     Full-text available via subscription  
Journal of Cardiopulmonary Rehabilitation and Prevention     Hybrid Journal   (Followers: 7)
Journal of Cardiothoracic and Vascular Anesthesia     Hybrid Journal   (Followers: 8)
Journal of Cardiothoracic Surgery     Open Access   (Followers: 5)
Journal of Cardiothoracic Trauma     Open Access  
Journal of Cardiothoracic-Renal Research     Full-text available via subscription  
Journal of Cardiovascular Computed Tomography     Hybrid Journal   (Followers: 2)
Journal of Cardiovascular Development and Disease     Open Access   (Followers: 1)
Journal of Cardiovascular Disease Research     Open Access   (Followers: 2)
Journal of Cardiovascular Diseases & Diagnosis     Open Access   (Followers: 1)
Journal of Cardiovascular Echography     Open Access   (Followers: 1)
Journal of Cardiovascular Electrophysiology     Hybrid Journal  
Journal Of Cardiovascular Emergencies     Open Access  
Journal of Cardiovascular Magnetic Resonance     Open Access   (Followers: 1)
Journal of Cardiovascular Medicine     Hybrid Journal   (Followers: 2)
Journal of Cardiovascular Medicine and Cardiology     Open Access   (Followers: 2)
Journal of Cardiovascular Nursing     Hybrid Journal   (Followers: 19)
Journal of Cardiovascular Pharmacology     Hybrid Journal   (Followers: 7)
Journal of Cardiovascular Pharmacology and Therapeutics     Hybrid Journal   (Followers: 2)
Journal of Cardiovascular Surgery     Full-text available via subscription   (Followers: 5)
Journal of Cardiovascular Translational Research     Hybrid Journal   (Followers: 2)
Journal of Clinical and Preventive Cardiology     Open Access   (Followers: 2)
Journal of Clinical Hypertension     Hybrid Journal   (Followers: 7)
Journal of Congenital Cardiology     Open Access   (Followers: 4)
Journal of Echocardiography     Hybrid Journal   (Followers: 5)
Journal of Electrocardiology     Hybrid Journal   (Followers: 1)
Journal of Endovascular Therapy     Full-text available via subscription   (Followers: 5)
Journal of Geriatric Cardiology     Open Access   (Followers: 4)
Journal of Human Hypertension     Hybrid Journal   (Followers: 3)
Journal of Hypertension     Hybrid Journal   (Followers: 13)
Journal of Indian College of Cardiology     Hybrid Journal  
Journal of Interventional Cardiac Electrophysiology     Hybrid Journal  
Journal of Interventional Cardiology     Open Access   (Followers: 2)
Journal of Molecular and Cellular Cardiology     Hybrid Journal   (Followers: 4)
Journal of Nuclear Cardiology     Hybrid Journal  
Journal of Rare Cardiovascular Diseases     Open Access   (Followers: 1)
Journal of Respiratory and CardioVascular Physical Therapy     Open Access   (Followers: 3)
Journal of Stroke and Cerebrovascular Diseases     Hybrid Journal   (Followers: 39)
Journal of the American College of Cardiology     Hybrid Journal   (Followers: 68)
Journal of the American Heart Association     Open Access   (Followers: 17)
Journal of the American Society of Echocardiography     Hybrid Journal   (Followers: 6)
Journal of the CardioMetabolic Syndrome     Hybrid Journal   (Followers: 1)
Journal of the Egyptian Society of Cardio-Thoracic Surgery     Open Access  
Journal of The Indian Academy of Echocardiography & Cardiovascular Imaging     Open Access   (Followers: 1)
Journal of the Practice of Cardiovascular Sciences     Open Access  
Journal of the Saudi Heart Association     Open Access  
Journal of Thoracic and Cardiovascular Surgery     Hybrid Journal   (Followers: 15)
Journal of Thrombosis and Haemostasis     Hybrid Journal   (Followers: 78)
Journal of Thrombosis and Thrombolysis     Hybrid Journal   (Followers: 34)
Journal of Vascular Access     Hybrid Journal   (Followers: 3)
Journal of Vascular Diagnostics     Open Access  
Journal of Veterinary Cardiology     Full-text available via subscription   (Followers: 7)
JRSM Cardiovascular Disease     Open Access  
Kardiologia Inwazyjna     Open Access  
Kardiologie up2date     Hybrid Journal   (Followers: 3)
Kerala Heart Journal     Open Access   (Followers: 1)
Microvascular Research     Hybrid Journal   (Followers: 2)
Monaldi Archives for Chest Disease     Open Access  
Nadciśnienie Tętnicze w Praktyce     Open Access  
Nature Reviews Cardiology     Full-text available via subscription   (Followers: 21)
Nepalese Heart Journal     Open Access  
Netherlands Heart Journal     Hybrid Journal   (Followers: 1)
Nigerian Journal of Cardiology     Open Access   (Followers: 1)
Nigerian Journal of Cardiovascular & Thoracic Surgery     Open Access  
Nutrition, Metabolism and Cardiovascular Diseases     Hybrid Journal   (Followers: 12)
Open Cardiovascular Medicine Journal     Open Access  
Open Heart     Open Access   (Followers: 1)
Open Hypertension Journal     Open Access  
Open Journal of Cardiovascular Surgery     Open Access   (Followers: 1)
Operative Techniques in Thoracic and Cardiovascular Surgery     Full-text available via subscription   (Followers: 2)
Pakistan Heart Journal     Open Access   (Followers: 2)
Parkinsonism & Related Disorders     Hybrid Journal   (Followers: 8)
Pediatric Cardiology     Hybrid Journal   (Followers: 10)
Platelets     Hybrid Journal   (Followers: 3)
Pregnancy Hypertension: An International Journal of Women's Cardiovascular Health     Hybrid Journal   (Followers: 4)
Prenatal Cardiology     Open Access   (Followers: 2)
Preventive Cardiology     Hybrid Journal   (Followers: 2)
Progress in Cardiovascular Diseases     Hybrid Journal   (Followers: 3)
Progress In Cardiovascular Nursing     Hybrid Journal  
Progress in Pediatric Cardiology     Full-text available via subscription   (Followers: 4)
Research in Cardiovascular Medicine     Open Access  
Research Journal of Cardiology     Open Access   (Followers: 1)
Research Reports in Clinical Cardiology     Open Access  
Resuscitation     Hybrid Journal   (Followers: 43)
Reviews in Vascular Medicine     Full-text available via subscription  
Revista Argentina de Cardiología     Open Access  
Revista Brasileira de Cardiologia Invasiva     Open Access  
Revista Brasileira de Cirurgia Cardiovascular     Open Access   (Followers: 1)
Revista Chilena de Cardiología     Open Access  
Revista Colombiana de Cardiologia     Open Access  
Revista Costarricense de Cardiología     Open Access  
Revista Cubana de Angiología y Cirugía Vascular     Open Access  
Revista Cubana de Cardiología y Cirugía Cardiovascular     Open Access  
Revista Española de Cardiología     Open Access  
Revista Española de Cardiología (English Edition)     Full-text available via subscription  
Revista Española de Cardiología Suplementos     Full-text available via subscription  
Revista Latinoamericana de Hipertension     Open Access  
Revista Portuguesa de Cardiologia     Open Access  
Revista Portuguesa de Cardiologia (English Edition)     Open Access  
Revista Uruguaya de Cardiologia     Open Access  
Russian Journal of Cardiology     Open Access  
SA Heart     Open Access  
Scandinavian Cardiovascular Journal     Hybrid Journal   (Followers: 2)
Seminars in Cardiothoracic and Vascular Anesthesia     Hybrid Journal   (Followers: 3)
Seminars in Cardiovascular Medicine     Open Access  
Seminars in Thoracic and Cardiovascular Surgery     Full-text available via subscription   (Followers: 5)
Seminars in Thoracic and Cardiovascular Surgery: Pediatric Cardiac Surgery Annual     Full-text available via subscription   (Followers: 6)
Seminars in Thrombosis and Hemostasis     Hybrid Journal   (Followers: 46)
Stroke     Hybrid Journal   (Followers: 94)
Stroke and Vascular Neurology     Open Access   (Followers: 3)
Structural Heart : The Journal of the Heart Team     Hybrid Journal  
Systemic Hypertension     Open Access  
Texas Heart Institute Journal     Open Access   (Followers: 2)
The VAD Journal     Open Access  
Therapeutic Advances in Cardiovascular Disease     Open Access  
Therapeutic Advances in Chronic Disease     Open Access   (Followers: 8)
Thoracic and Cardiovascular Surgeon     Hybrid Journal   (Followers: 2)
Thoracic and Cardiovascular Surgeon Reports     Open Access   (Followers: 2)
Trends in Cardiovascular Medicine     Hybrid Journal   (Followers: 4)
Trials     Open Access   (Followers: 4)
University Heart Journal     Open Access   (Followers: 1)
US Cardiology Review     Open Access   (Followers: 1)
Vascular and Endovascular Review     Open Access   (Followers: 1)
World Journal for Pediatric and Congenital Heart Surgery     Hybrid Journal   (Followers: 4)
World Journal of Cardiovascular Diseases     Open Access   (Followers: 2)
World Journal of Cardiovascular Surgery     Open Access   (Followers: 2)
Zeitschrift für Komplementärmedizin     Hybrid Journal  

  First | 1 2     

Similar Journals
Journal Cover
Journal of Cardiovascular Pharmacology
Journal Prestige (SJR): 0.917
Citation Impact (citeScore): 2
Number of Followers: 7  
 
  Hybrid Journal Hybrid journal (It can contain Open Access articles)
ISSN (Print) 0160-2446 - ISSN (Online) 1533-4023
Published by LWW Wolters Kluwer Homepage  [299 journals]
  • Myocardial Phosphodiesterases and Their Role in cGMP Regulation
    • Authors: Dunkerly-Eyring; Brittany; Kass, David A.
      Abstract: imageAbstract: Cyclic nucleotide phosphodiesterases comprise an 11-member superfamily yielding near 100 isoform variants that hydrolyze cAMP or cGMP to their respective 5′-monophosphate form. Each plays a role in compartmentalized cyclic nucleotide signaling, with varying selectivity for each substrate, and conveying cell and intracellular-specific localized control. This review focuses on the 5 phosphodiesterases (PDEs) expressed in the cardiac myocyte capable of hydrolyzing cGMP and that have been shown to play a role in cardiac physiological and pathological processes. PDE1, PDE2, and PDE3 catabolize cAMP as well, whereas PDE5 and PDE9 are cGMP selective. PDE3 and PDE5 are already in clinical use, the former for heart failure, and PDE1, PDE9, and PDE5 are all being actively studied for this indication in patients. Research in just the past few years has revealed many novel cardiac influences of each isoform, expanding the therapeutic potential from their selective pharmacological blockade or in some instances, activation. PDE1C inhibition was found to confer cell survival protection and enhance cardiac contractility, whereas PDE2 inhibition or activation induces beneficial effects in hypertrophied or failing hearts, respectively. PDE3 inhibition is already clinically used to treat acute decompensated heart failure, although toxicity has precluded its long-term use. However, newer approaches including isoform-specific allosteric modulation may change this. Finally, inhibition of PDE5A and PDE9A counter pathological remodeling of the heart and are both being pursued in clinical trials. Here, we discuss recent research advances in each of these PDEs, their impact on the myocardium, and cardiac therapeutic potential.
      PubDate: Mon, 01 Jun 2020 00:00:00 GMT-
       
  • Targets of cGMP/cGKI in Cardiac Myocytes
    • Authors: Adler; Julia; Kuret, Anna; Längst, Natalie; Lukowski, Robert
      Abstract: imageAbstract: The 3′,5′-cyclic guanosine monophosphate (cGMP)-dependent protein kinase type I (cGKI aka PKGI) is a major cardiac effector acting downstream of nitric oxide (NO)-sensitive soluble guanylyl cyclase and natriuretic peptides (NPs), which signal through transmembrane guanylyl cyclases. Consistent with the wide distribution of the cGMP-generating guanylyl cyclases, cGKI, which usually elicits its cellular effects by direct phosphorylation of its targets, is present in multiple cardiac cell types including cardiomyocytes (CMs). Although numerous targets of cGMP/cGKI in heart were identified in the past, neither their exact patho-/physiological functions nor cell-type specific roles are clear. Herein, we inform about the current knowledge on the signal transduction downstream of CM cGKI. We believe that better insights into the specific actions of cGMP and cGKI in these cells will help to guide future studies in the search for predictive biomarkers for the response to pharmacological cGMP pathway modulation. In addition, targets downstream of cGMP/cGKI may be exploited for refined and optimized diagnostic and therapeutic strategies in different types of heart disease and their causes. Importantly, key functions of these proteins and particularly sites of regulatory phosphorylation by cGKI should, at least in principle, remain intact, although upstream signaling through the second messenger cGMP is impaired or dysregulated in a stressed or diseased heart state.
      PubDate: Mon, 01 Jun 2020 00:00:00 GMT-
       
  • Nitric Oxide in Post-cardiac Arrest Syndrome
    • Authors: Miyazaki; Yusuke; Ichinose, Fumito
      Abstract: imageAbstract: Sudden cardiac arrest is a leading cause of death worldwide. Although the methods of cardiopulmonary resuscitation have been improved, mortality is still unacceptably high, and many survivors suffer from lasting neurological deficits due to the post-cardiac arrest syndrome (PCAS). Pathophysiologically, generalized vascular endothelial dysfunction accompanied by platelet activation and systemic inflammation has been implicated in the pathogenesis of PCAS. Because endothelial-derived nitric oxide (NO) plays a central role in maintaining vascular homeostasis, the role of NO-dependent signaling has been a focus of the intense investigation. Recent preclinical studies showed that therapeutic interventions that increase vascular NO bioavailability may improve outcomes after cardiac arrest complicated with PCAS. In particular, NO inhalation therapy has been shown to improve neurological outcomes and survival in multiple species. Clinical studies examining the safety and efficacy of inhaled NO in patients sustaining PCAS are warranted.
      PubDate: Mon, 01 Jun 2020 00:00:00 GMT-
       
  • cGMP Signaling in Cardiovascular Diseases: Linking Genotype and Phenotype
    • Authors: Dang; Tan An; Schunkert, Heribert; Kessler, Thorsten
      Abstract: imageAbstract: Cyclic guanosine 3′,5′-monophosphate (cGMP) is the key second messenger molecule in nitric oxide signaling. Its rapid generation and fate, but also its role in mediating acute cellular functions has been extensively studied. In the past years, genetic studies suggested an important role for cGMP in affecting the risk of chronic cardiovascular diseases, for example, coronary artery disease and myocardial infarction. Here, we review the role of cGMP in atherosclerosis and other cardiovascular diseases and discuss recent genetic findings and identified mechanisms. Finally, we highlight open questions and promising research topics.
      PubDate: Mon, 01 Jun 2020 00:00:00 GMT-
       
  • Cardiovascular Pharmacology in the Time of COVID-19: A Focus on
           Angiotensin-Converting Enzyme 2
    • Authors: Buckley; Leo F.; Cheng, Judy W. M.; Desai, Akshay
      Abstract: imageAbstract: Coronavirus disease-2019 (COVID-19) has emerged as a pandemic affecting millions of adults. Severe acute respiratory syndrome coronavirus-2019 (SARS-CoV-2), the causative virus of COVID-19, infects host cells through angiotensin-converting enzyme 2 (ACE2). Preclinical models suggest that ACE2 upregulation confers protective effects in acute lung injury. In addition, renin–angiotensin aldosterone system inhibitors reduce adverse atherosclerotic cardiovascular disease, heart failure, and chronic kidney disease outcomes, but may increase ACE2 levels. We review current knowledge of the role of ACE2 in cardiovascular physiology and SARS-CoV-2 virology, as well as clinical data to inform the management of patients with or at risk for COVID-19 who require renin–angiotensin–aldosterone system inhibitor therapy.
      PubDate: Mon, 01 Jun 2020 00:00:00 GMT-
       
  • Direct Oral Anticoagulants for the Treatment of Left Ventricular
           Thrombus—A New Indication' A Meta-summary of Case Reports
    • Authors: Tomasoni; Daniela; Sciatti, Edoardo; Bonelli, Andrea; Vizzardi, Enrico; Metra, Marco
      Abstract: imageAbstract: Left ventricular thrombus (LVT) can be a consequence of cardiac diseases such as heart failure with reduced ejection fraction and acute myocardial infarction. Currently, the guidelines recommend the use of warfarin for the treatment of this condition. However, there are increasing reports of patients with LVTs being treated with direct oral anticoagulants (DOACs), for several reasons. We set out to review the available literature to assess the safety and the efficacy of this approach. We analyzed 52 cases, extrapolated by 34 papers contained in literature, focusing on the characteristics of patients, treatment, outcome, and follow-up. Rivaroxaban was the most commonly used DOAC, followed by apixaban. The diagnosis of LVT and the follow-up were mainly performed by transthoracic echocardiography. The thrombus resolved in 45 patients (92%) of 49 (there are no data available regarding the outcome of 3 patients) and failed to resolve in 4 patients treated with DOACs. The resolution occurred in a median of 32 days. DOACs are shown to be a reasonable and valid option for the treatment of LVT. Our study provides a rationale for a prospective randomized controlled trial.
      PubDate: Mon, 01 Jun 2020 00:00:00 GMT-
       
  • Higenamine Improves Cardiac and Renal Fibrosis in Rats With Cardiorenal
           Syndrome via ASK1 Signaling Pathway
    • Authors: Deng; Ting; Wei, Zhenming; Gael, Akindavyi; Deng, Xiaofang; Liu, Yunfeng; Lai, Jun; Hang, Liwei; Yan, Quanneng; Fu, Qiang; Li, Zhiliang
      Abstract: imageAbstract: The pathogenesis of cardiorenal syndrome (CRS) is very complex, and currently there is no effective treatment for CRS. Higenamine (HI) has been shown to improve cardiac function in rats with heart failure. However, the role of higenamine in CRS remains unknown. Here, in vitro, higenamine treatment markedly reduced neonatal rat cardiac fibroblast collagen synthesis and inhibited neonatal rat cardiac myocyte hypertrophy. In our study, a rat model of type 2 CRS was induced by left anterior descending coronary artery ligation combined with 5/6 subtotal nephrectomy (STNx). Higenamine treatment decreased serum creatinine (Scr), blood urea nitrogen, and brain natriuretic peptide levels and was capable of improving left ventricular remodeling and systolic function in CRS rats, accompanied with decreased expression of transforming growth factor-β1 (TGF-β1), α–smooth muscle actin (α-SMA) and collagen I (Col1A1). Moreover, higenamine significantly inhibited the protein expression of phosphorylated apoptosis signal-regulated kinase 1 (p-ASK1) and downstream mitogen-activated protein kinases (MAPK) (ERK, P38)/NF-κB in cardiorenal tissues of CRS rats and neonatal rat cardiac fibroblast/neonatal rat cardiac myocyte cells. Our study demonstrated that higenamine improved cardiorenal function in CRS rats and attenuated heart and kidney fibrosis possibly via targeting ASK1/MAPK (ERK, P38)/NF-κB signaling pathway. This finding extends our knowledge on the role of higenamine in cardiorenal fibrosis, providing a potential target to prevent the progression of CRS.
      PubDate: Mon, 01 Jun 2020 00:00:00 GMT-
       
  • Ursolic Acid Improves Monocrotaline-Induced Right Ventricular Remodeling
           by Regulating Metabolism
    • Authors: Gao; Xiaojian; Zhang, Zeyu; Li, Xin; Wei, Qingxia; Li, Hanlu; Li, Chen; Chen, Haixu; Liu, Chunlei; He, Kunlun
      Abstract: imageAbstract: Pulmonary arterial hypertension (PAH) is a progressive and malignant disease characterized by pulmonary small arteries and right ventricle (RV) remodeling that can lead to severe RV dysfunction and death. The current therapeutic targets for RV dysfunction, which is strongly linked to mortality, are far from adequate. Therefore, we investigated the effect of ursolic acid (UA), a pentacyclic triterpenoid carboxylic acid, on PAH-induced RV remodeling and its underlying mechanism. We established a PAH model by injecting Sprague Dawley rats with monocrotaline (MCT, 60 mg/kg, ip), as verified by echocardiography and hemodynamic examination. Proteomic analysis was performed on RV samples using a Q Exactive high-field mass spectrometer, followed by KEGG enrichment analysis. The effect of 4 weeks of UA (50 mg/kg) treatment on RV remodeling was explored based on ultrasound, hemodynamic parameters, and histological changes, with the mechanism verified in vivo and in vitro by qRT-PCR and western blotting. RV hypertrophy, fibrosis, increased apoptosis, and abnormal metabolism were induced by MCT and suppressed by UA via a mechanism that changed the expression of key markers. UA also attenuated the Phenylephrine-induced hypertrophy of neonatal rat ventricular myocytes and upregulated peroxisome proliferator-activated receptor-alpha (PPARα), a key fatty acid metabolism regulator, and its downstream factor carnitine palmitoyl transferase 1b. In conclusion, UA exerts beneficial effects on PAH-induced RV dysfunction and remodeling by regulating PPARα-dependent fatty acid metabolism.
      PubDate: Mon, 01 Jun 2020 00:00:00 GMT-
       
  • Inhibition of GPR35 Preserves Mitochondrial Function After Myocardial
           Infarction by Targeting Calpain 1/2
    • Authors: Chen; Ken; He, Lei; Li, Yong; Li, Xiuchuan; Qiu, Chenming; Pei, Haifeng; Yang, Dachun
      Abstract: imageAbstract: Ischemia and anoxia-induced mitochondrial impairment may be a key factor leading to heart injury during myocardial infarction (MI). Calpain 1 and 2 are involved in the MI-induced mitochondria injury. G protein-coupled receptor 35 (GPR35) could be triggered by hypoxia. Whether or not GPR35 regulates calpain 1/2 in the pathogenesis of MI is still unclear. In this study, we determined that MI increases GPR35 expression in myocardial tissue. Suppression of GPR35 protects heart from MI injury in mice through reduction of reactive oxygen species activity and mitochondria-dependent apoptosis. Further studies show that GPR35 regulates calpain 1/2. Suppression of GPR35 reduces the expression and activity of calpain 1/2, and alleviates calpain 1/2-associated mitochondrial injury to preserve cardiac function. Based on these data, we conclude that a functional inhibition of GPR35 downregulates calpain 1/2 and contributes to maintenance of cardiac function under pathologic conditions with mitochondrial disorder. In conclusion, our study showed that the identified regulation by GPR35 of calpain 1/2 has important implications for the pathogenesis of MI. Targeting the action of GPR35 and calpain 1/2 in mitochondria presents a potential therapeutic intervention for MI.
      PubDate: Mon, 01 Jun 2020 00:00:00 GMT-
       
  • Cardioprotective Effects of Latifolin Against Doxorubicin-Induced
           Cardiotoxicity by Macrophage Polarization in Mice
    • Authors: Zhang; Ni; Shou, Binyao; Chen, Lanying; Lai, Xiaoxiao; Luo, Yingying; Meng, Xiaowei; Liu, Ronghua
      Abstract: imageAbstract: Latifolin, one of the major flavonoids extracted from lignum dalbergiae odoriferae, has been documented to protect the heart from acute myocardial ischemia induced by pituitrin and isoproterenol in rats and has also been found to inhibit inflammation. In this study, we aimed to investigate whether latifolin could protect the heart from doxorubicin (DOX)-induced cardiotoxicity and elucidate its underlying mechanisms. Male mice were treated with an intraperitoneal dose of DOX (20 mg/kg) plus oral latifolin at a dose of 50 or 100 mg/kg for 12 days. After exposure, we assessed cardiac function, myocardial injury, and macrophage polarization in excised cardiac tissue. Our results demonstrated that latifolin prevented DOX-induced cardiac dysfunction and produced macrophage polarization in mice challenged with latifolin. In cultured peritoneal macrophages, latifolin significantly reduced inflammatory cytokines (P < 0.05). Furthermore, latifolin remarkably decreased the percentage of macrophage M1/M2 polarization (P < 0.05). The results from the present study highlight the benefits of treatment with latifolin in DOX-induced cardiotoxicity, and the mechanism involved in mediating the polarization phenotype change of M1/M2 macrophages.
      PubDate: Mon, 01 Jun 2020 00:00:00 GMT-
       
  • Preventive Beneficial Effect of an Aqueous Extract of Phyllanthus amarus
           Schum. and Thonn. (Euphorbiaceae) on DOCA-Salt–Induced Hypertension,
           Cardiac Hypertrophy and Dysfunction, and Endothelial Dysfunction in Rats
    • Authors: Yao; N'guessan Alain; Niazi, Zahid Rasul; Najmanová, Iveta; Kamagaté, Mamadou; Said, Amissi; Chabert, Philippe; Auger, Cyril; Die-Kakou, Henri; Schini-Kerth, Valérie
      Abstract: imageAbstract: This study investigated the preventive effect of an aqueous extract of the whole plant of Phyllanthus amarus (AEPA) on blood pressure, cardiac, and endothelial function in the deoxycorticosterone acetate (DOCA) salt–induced hypertensive rat model. Male Wistar rats were assigned into 5 groups receiving either vehicle (control and DOCA salt), DOCA salt combined with AEPA at 100 or 300 mg/kg, or AEPA (100 mg/kg) alone for 5 weeks. In addition, DOCA salt–treated rats were allowed free access to water containing 1% NaCl. Systolic blood pressure, left ventricle parameters, vascular reactivity of primary mesenteric artery rings, the vascular level of oxidative stress, and the level of target proteins were determined, using respectively tail-cuff sphygmomanometry, echocardiography, organ chambers, dihydroethidium staining, and immunofluorescence methods. After 5 weeks, AEPA treatments (100 or 300 mg/kg per day) significantly prevented the increase in systolic blood pressure in DOCA salt–treated rats, respectively, by about 24 and 21 mm Hg, improved cardiac diastolic function, and reduced significantly the increased posterior and septum diastolic wall thickness and the left ventricle mass in hypertensive rats. Moreover, the DOCA salt–induced endothelial dysfunction and the blunted nitric oxide- and endothelium-dependent hyperpolarization-mediated relaxations in primary mesenteric artery were improved after the AEPA treatments. AEPA also reduced the level of vascular oxidative stress and the expression level of target proteins (eNOS, COX-2, NADPH oxidase subunit p22phox) in DOCA salt rats. Altogether, AEPA prevented hypertension, improved cardiac structure and function, and improved endothelial function in DOCA salt rats. Such beneficial effects seem to be related, at least in part, to normalization of the vascular level of oxidative stress.
      PubDate: Mon, 01 Jun 2020 00:00:00 GMT-
       
  • Rosuvastatin Reverses Hypertension-Induced Changes in the Aorta Structure
           and Endothelium-Dependent Relaxation in Rats Through Suppression of
           Apoptosis and Inflammation
    • Authors: Lv; Qingbo; Wang, Yao; Li, Ya; Zhao, Liding; Gong, Yingchao; Wang, Meihui; Wang, Min; Fu, Guosheng; Zhang, Wenbin
      Abstract: imageAbstract: Vascular remodeling is one of the most critical complications caused by hypertension. Previous studies have demonstrated that rosuvastatin has anti-inflammatory, antioxidant, and antiplatelet effects and therefore can be used to treat cardiovascular disease. In this study, we explored the beneficial effects of rosuvastatin in reversing aortic remodeling in spontaneously hypertensive rats. After treating with different doses of rosuvastatin, its antilipid, antiapoptosis, and anti-inflammatory effects were determined. We also examined whether rosuvastatin can improve the structure and function of the aorta. We found that rosuvastatin treatment of spontaneously hypertensive rats for 2 months at 2 different doses can effectively reduce the media thickness of the aorta compared with the control group. Similarly, rosuvastatin improved the vascular relaxation function of the aortic rings at a high level of acetylcholine in vitro. Mechanistically, it was found that rosuvastatin increased the expression of endothelial nitric oxide synthase and plasma nitrite/nitrate levels. Besides, rosuvastatin suppressed the apoptosis and inflammation and upregulated the expression of gap-junction complex connexin 43 both in media and endothelium. Finally, rosuvastatin inhibited the AT1R/PKCα/HSP70 signaling transduction pathway. In summary, these findings demonstrated that rosuvastatin could improve the vascular structure and function mainly by increasing endothelial nitric oxide synthase expression and preventing apoptosis and inflammation. This study provided evidence that rosuvastatin has beneficial effects in reversing the remodeling of the aorta due to hypertension.
      PubDate: Mon, 01 Jun 2020 00:00:00 GMT-
       
  • Chrysin Alleviates Monocrotaline-Induced Pulmonary Hypertension in Rats
           Through Regulation of Intracellular Calcium Homeostasis in Pulmonary
           Arterial Smooth Muscle Cells
    • Authors: Dong; Fang; Zhang, Jun; Chen, Xiuqing; Zhang, Suya; Zhu, Licheng; Peng, Yufei; Guo, Zhiping
      Abstract: imageAbstract: Chrysin (CH) is the main ingredient of many medicinal plants. Our previous study showed that CH could suppress hypoxia-induced pulmonary arterial smooth muscle cells proliferation and alleviate chronic hypoxia-induced pulmonary hypertension by targeting store-operated Ca2+ entry (SOCE)-[Ca2+]i pathway. In this study, we investigated the effect of CH on monocrotaline-induced pulmonary hypertension (MCTPH) and the mechanism behind it. Results show that, in MCTPH model rats, (1) CH significantly reduced the enhancement of right ventricular pressure, right ventricular hypertrophy, and pulmonary vascular remodeling; (2) CH markedly suppressed the promotion of SOCE and [Ca2+]i in pulmonary arterial smooth muscle cells; and (3) CH obviously inhibited the MCT-upregulated proliferating cell nuclear antigen, TRPC1, TRPC4, and TRPC6 expression in distal pulmonary arteries. These results demonstrate that CH likely alleviates MCTPH by targeting TRPC1,4,6-SOCE-[Ca2+]i pathway.
      PubDate: Mon, 01 Jun 2020 00:00:00 GMT-
       
  • Transduction Efficiency of Adenovirus Vectors in Endothelial Cells and
           Vascular Smooth Muscle Cells
    • Authors: Mokhashi; Nikita; Choi, Robert Y.; Cicalese, Stephanie; Eguchi, Kunie; Boyer, Michael J.; Cooper, Hannah A.; Kimura, Yayoi; Akiyama, Tomoko; Scalia, Rosario; Rizzo, Victor; Eguchi, Satoru
      Abstract: imageAbstract: Adenoviral vectors are useful tools in manipulating a gene of interest in vitro and in vivo, including in the vascular system. The transduction efficiencies of adenoviral vectors in vascular cells such as endothelial cells (ECs) and vascular smooth muscle cells (VSMCs) are known to be lower than those in epithelial cell types. The effective entry for adenoviral vectors is primarily mediated through the coxsackievirus and adenovirus receptor (CAR), which has been shown to be expressed in both cell types. Cationic liposomes have been used to enhance adenovirus transduction efficiency in nonepithelial cells. Accordingly, the aim of this study is to obtain new information regarding differences in transduction efficiencies, cationic liposome sensitivity, and CAR expression between ECs and VSMCs. Using cultured rat aortic ECs and VSMCs, here, we have compared transduction efficiency of adenoviruses with or without inclusion of liposomes and CAR expression. A significant increase in basal transduction efficiency was observed in ECs compared with VSMCs. Cationic liposome polybrene enhanced transduction efficiency in VSMCs, whereas decreased efficiency was observed in ECs. Western blotting demonstrated expression of the CAR in ECs but not in VSMCs. Proteomic analysis and mouse aorta immunostaining further suggests significant expression of the CAR in ECs but not in VSMCs. In conclusion, adenoviruses can effectively transduce the gene of interest in aortic ECs likely because of abundant expression of the CAR, whereas cationic liposomes such as polybrene enhance the transduction efficiency in VSMCs lacking CAR expression.
      PubDate: Mon, 01 Jun 2020 00:00:00 GMT-
       
 
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