Subjects -> MEDICAL SCIENCES (Total: 8642 journals)
    - ANAESTHESIOLOGY (120 journals)
    - CARDIOVASCULAR DISEASES (338 journals)
    - DENTISTRY (293 journals)
    - ENDOCRINOLOGY (150 journals)
    - FORENSIC SCIENCES (42 journals)
    - HEMATOLOGY (157 journals)
    - HYPNOSIS (4 journals)
    - INTERNAL MEDICINE (174 journals)
    - MEDICAL GENETICS (58 journals)
    - MEDICAL SCIENCES (2392 journals)
    - NURSES AND NURSING (364 journals)
    - OBSTETRICS AND GYNECOLOGY (207 journals)
    - ONCOLOGY (384 journals)
    - OTORHINOLARYNGOLOGY (83 journals)
    - PATHOLOGY (100 journals)
    - PEDIATRICS (275 journals)
    - PSYCHIATRY AND NEUROLOGY (833 journals)
    - RESPIRATORY DISEASES (104 journals)
    - RHEUMATOLOGY (79 journals)
    - SPORTS MEDICINE (81 journals)
    - SURGERY (406 journals)

CARDIOVASCULAR DISEASES (338 journals)                  1 2 | Last

Showing 1 - 200 of 338 Journals sorted alphabetically
Acta Angiologica     Open Access   (Followers: 5)
Acta Cardiologica     Hybrid Journal   (Followers: 2)
Acute Cardiac Care     Hybrid Journal   (Followers: 8)
Adipositas - Ursachen, Folgeerkrankungen, Therapie     Hybrid Journal  
AJP Heart and Circulatory Physiology     Hybrid Journal   (Followers: 12)
Aktuelle Kardiologie     Hybrid Journal   (Followers: 1)
American Heart Journal     Hybrid Journal   (Followers: 60)
American Journal of Cardiology     Hybrid Journal   (Followers: 68)
American Journal of Cardiovascular Drugs     Hybrid Journal   (Followers: 17)
American Journal of Hypertension     Hybrid Journal   (Followers: 28)
Anales de Cirugia Vascular     Full-text available via subscription   (Followers: 1)
Anatolian Journal of Cardiology     Open Access   (Followers: 6)
Angiología     Full-text available via subscription  
Angiologia e Cirurgia Vascular     Open Access   (Followers: 1)
Angiology     Hybrid Journal   (Followers: 3)
Annales de Cardiologie et d'Angéiologie     Full-text available via subscription   (Followers: 1)
Annals of Circulation     Open Access   (Followers: 2)
Annals of Noninvasive Electrocardiology     Hybrid Journal   (Followers: 1)
Annals of Pediatric Cardiology     Open Access   (Followers: 12)
AORTA     Open Access  
Archives of Cardiovascular Diseases     Full-text available via subscription   (Followers: 5)
Archives of Cardiovascular Diseases Supplements     Full-text available via subscription   (Followers: 3)
Archives of Cardiovascular Imaging     Open Access   (Followers: 2)
Archivos de cardiología de México     Open Access   (Followers: 1)
Argentine Journal of Cardiology (English edition)     Open Access   (Followers: 2)
Arquivos Brasileiros de Cardiologia     Open Access   (Followers: 2)
Arrhythmia & Electrophysiology Review     Open Access   (Followers: 1)
Arteriosclerosis, Thrombosis and Vascular Biology     Full-text available via subscription   (Followers: 32)
Artery Research     Hybrid Journal   (Followers: 4)
ARYA Atherosclerosis     Open Access  
ASAIO Journal     Hybrid Journal   (Followers: 3)
ASEAN Heart Journal     Open Access   (Followers: 2)
Asian Cardiovascular and Thoracic Annals     Hybrid Journal   (Followers: 2)
Aswan Heart Centre Science & Practice Services     Open Access   (Followers: 1)
Atherosclerosis : X     Open Access  
Bangladesh Heart Journal     Open Access   (Followers: 3)
Basic Research in Cardiology     Hybrid Journal   (Followers: 10)
BMC Cardiovascular Disorders     Open Access   (Followers: 22)
Brain Circulation     Open Access   (Followers: 1)
British Journal of Cardiology     Full-text available via subscription   (Followers: 18)
Canadian Journal of Cardiology     Hybrid Journal   (Followers: 18)
Cardiac Cath Lab Director     Full-text available via subscription  
Cardiac Electrophysiology Review     Hybrid Journal   (Followers: 2)
Cardiac Failure Review     Open Access   (Followers: 1)
Cardiocore     Full-text available via subscription   (Followers: 1)
Cardiogenetics     Open Access   (Followers: 3)
Cardiology     Full-text available via subscription   (Followers: 20)
Cardiology and Angiology: An International Journal     Open Access   (Followers: 1)
Cardiology and Therapy     Open Access   (Followers: 12)
Cardiology Clinics     Full-text available via subscription   (Followers: 14)
Cardiology in Review     Hybrid Journal   (Followers: 8)
Cardiology in the Young     Hybrid Journal   (Followers: 34)
Cardiology Journal     Open Access   (Followers: 6)
Cardiology Plus     Open Access   (Followers: 1)
Cardiology Research     Open Access   (Followers: 15)
Cardiology Research and Practice     Open Access   (Followers: 10)
Cardiopulmonary Physical Therapy Journal     Hybrid Journal   (Followers: 8)
Cardiorenal Medicine     Full-text available via subscription   (Followers: 1)
Cardiothoracic Surgeon     Open Access   (Followers: 1)
CardioVasc     Full-text available via subscription   (Followers: 1)
Cardiovascular & Haematological Disorders - Drug Targets     Hybrid Journal   (Followers: 1)
Cardiovascular & Hematological Agents in Medicinal Chemistry     Hybrid Journal   (Followers: 2)
CardioVascular and Interventional Radiology     Hybrid Journal   (Followers: 15)
Cardiovascular and Thoracic Open     Open Access  
Cardiovascular Diabetology     Open Access   (Followers: 10)
Cardiovascular Drugs and Therapy     Hybrid Journal   (Followers: 14)
Cardiovascular Endocrinology & Metabolism     Hybrid Journal   (Followers: 1)
Cardiovascular Engineering     Hybrid Journal   (Followers: 1)
Cardiovascular Engineering and Technology     Hybrid Journal   (Followers: 1)
Cardiovascular Intervention and Therapeutics     Hybrid Journal   (Followers: 5)
Cardiovascular Journal     Open Access   (Followers: 6)
Cardiovascular Journal of Africa     Full-text available via subscription   (Followers: 5)
Cardiovascular Journal of South Africa     Full-text available via subscription   (Followers: 1)
Cardiovascular Medicine in General Practice     Full-text available via subscription   (Followers: 7)
Cardiovascular Pathology     Hybrid Journal   (Followers: 4)
Cardiovascular Regenerative Medicine     Open Access  
Cardiovascular Research     Hybrid Journal   (Followers: 15)
Cardiovascular Revascularization Medicine     Hybrid Journal   (Followers: 1)
Cardiovascular System     Open Access  
Cardiovascular Therapeutics     Open Access   (Followers: 1)
Cardiovascular Toxicology     Hybrid Journal   (Followers: 6)
Cardiovascular Ultrasound     Open Access   (Followers: 5)
Case Reports in Cardiology     Open Access   (Followers: 7)
Catheterization and Cardiovascular Interventions     Hybrid Journal   (Followers: 3)
Cerebrovascular Diseases     Full-text available via subscription   (Followers: 3)
Cerebrovascular Diseases Extra     Open Access  
Chest     Full-text available via subscription   (Followers: 103)
Choroby Serca i Naczyń     Open Access   (Followers: 1)
Circulation     Hybrid Journal   (Followers: 265)
Circulation : Cardiovascular Imaging     Hybrid Journal   (Followers: 15)
Circulation : Cardiovascular Interventions     Hybrid Journal   (Followers: 19)
Circulation : Cardiovascular Quality and Outcomes     Hybrid Journal   (Followers: 11)
Circulation : Genomic and Precision Medicine     Hybrid Journal   (Followers: 16)
Circulation : Heart Failure     Hybrid Journal   (Followers: 26)
Circulation Research     Hybrid Journal   (Followers: 36)
Cirugía Cardiovascular     Open Access  
Clínica e Investigación en Arteriosclerosis     Full-text available via subscription  
Clínica e Investigación en arteriosclerosis (English Edition)     Hybrid Journal  
Clinical and Experimental Hypertension     Hybrid Journal   (Followers: 3)
Clinical Cardiology     Hybrid Journal   (Followers: 11)
Clinical Hypertension     Open Access   (Followers: 5)
Clinical Medicine Insights : Cardiology     Open Access   (Followers: 6)
Clinical Research in Cardiology     Hybrid Journal   (Followers: 6)
Clinical Research in Cardiology Supplements     Hybrid Journal  
Clinical Trials and Regulatory Science in Cardiology     Open Access   (Followers: 4)
Congenital Heart Disease     Hybrid Journal   (Followers: 6)
Congestive Heart Failure     Hybrid Journal   (Followers: 4)
Cor et Vasa     Full-text available via subscription   (Followers: 1)
Coronary Artery Disease     Hybrid Journal   (Followers: 2)
CorSalud     Open Access  
Critical Pathways in Cardiology     Hybrid Journal   (Followers: 4)
Current Cardiology Reports     Hybrid Journal   (Followers: 7)
Current Cardiology Reviews     Hybrid Journal   (Followers: 4)
Current Cardiovascular Imaging Reports     Hybrid Journal   (Followers: 1)
Current Cardiovascular Risk Reports     Hybrid Journal  
Current Heart Failure Reports     Hybrid Journal   (Followers: 5)
Current Hypertension Reports     Hybrid Journal   (Followers: 6)
Current Hypertension Reviews     Hybrid Journal   (Followers: 6)
Current Opinion in Cardiology     Hybrid Journal   (Followers: 14)
Current Problems in Cardiology     Hybrid Journal   (Followers: 3)
Current Research : Cardiology     Full-text available via subscription   (Followers: 1)
Current Treatment Options in Cardiovascular Medicine     Hybrid Journal   (Followers: 1)
Current Vascular Pharmacology     Hybrid Journal   (Followers: 5)
CVIR Endovascular     Open Access   (Followers: 1)
Der Kardiologe     Hybrid Journal   (Followers: 2)
Echo Research and Practice     Open Access   (Followers: 2)
Echocardiography     Hybrid Journal   (Followers: 4)
Egyptian Heart Journal     Open Access   (Followers: 2)
Egyptian Journal of Cardiothoracic Anesthesia     Open Access  
ESC Heart Failure     Open Access   (Followers: 4)
European Cardiology Review     Open Access   (Followers: 1)
European Heart Journal     Hybrid Journal   (Followers: 68)
European Heart Journal - Cardiovascular Imaging     Hybrid Journal   (Followers: 10)
European Heart Journal - Cardiovascular Pharmacotherapy     Full-text available via subscription   (Followers: 2)
European Heart Journal - Quality of Care and Clinical Outcomes     Hybrid Journal  
European Heart Journal : Acute Cardiovascular Care     Hybrid Journal   (Followers: 1)
European Heart Journal : Case Reports     Open Access   (Followers: 1)
European Heart Journal Supplements     Hybrid Journal   (Followers: 8)
European Journal of Cardio-Thoracic Surgery     Hybrid Journal   (Followers: 9)
European Journal of Cardio-Thoracic Surgery Supplements     Full-text available via subscription   (Followers: 2)
European Journal of Cardiovascular Nursing     Hybrid Journal   (Followers: 5)
European Journal of Heart Failure     Hybrid Journal   (Followers: 14)
European Journal of Preventive Cardiology.     Hybrid Journal   (Followers: 6)
European Stroke Organisation     Hybrid Journal   (Followers: 3)
Experimental & Translational Stroke Medicine     Open Access   (Followers: 9)
Expert Review of Cardiovascular Therapy     Full-text available via subscription   (Followers: 3)
Folia Cardiologica     Open Access  
Forum Zaburzeń Metabolicznych     Hybrid Journal  
Frontiers in Cardiovascular Medicine     Open Access   (Followers: 1)
Future Cardiology     Hybrid Journal   (Followers: 6)
General Thoracic and Cardiovascular Surgery     Hybrid Journal   (Followers: 3)
Global Cardiology Science and Practice     Open Access   (Followers: 5)
Global Heart     Hybrid Journal   (Followers: 3)
Heart     Hybrid Journal   (Followers: 48)
Heart and Mind     Open Access  
Heart and Vessels     Hybrid Journal  
Heart Failure Clinics     Full-text available via subscription   (Followers: 2)
Heart Failure Reviews     Hybrid Journal   (Followers: 3)
Heart India     Open Access   (Followers: 2)
Heart International     Full-text available via subscription  
Heart Rhythm     Hybrid Journal   (Followers: 11)
Heart Views     Open Access   (Followers: 2)
HeartRhythm Case Reports     Open Access  
Hellenic Journal of Cardiology     Open Access   (Followers: 1)
Herz     Hybrid Journal   (Followers: 3)
High Blood Pressure & Cardiovascular Prevention     Full-text available via subscription   (Followers: 2)
Hypertension     Full-text available via subscription   (Followers: 23)
Hypertension     Open Access   (Followers: 2)
Hypertension in Pregnancy     Hybrid Journal   (Followers: 9)
Hypertension Research     Hybrid Journal   (Followers: 4)
Ibrahim Cardiac Medical Journal     Open Access  
IJC Heart & Vessels     Open Access   (Followers: 1)
IJC Heart & Vasculature     Open Access   (Followers: 1)
IJC Metabolic & Endocrine     Open Access   (Followers: 1)
Indian Heart Journal     Open Access   (Followers: 5)
Indian Journal of Cardiovascular Disease in Women WINCARS     Open Access  
Indian Journal of Thoracic and Cardiovascular Surgery     Hybrid Journal  
Indian Pacing and Electrophysiology Journal     Open Access   (Followers: 1)
Innovations : Technology and Techniques in Cardiothoracic and Vascular Surgery     Hybrid Journal   (Followers: 1)
Insuficiencia Cardíaca     Open Access  
Interactive CardioVascular and Thoracic Surgery     Hybrid Journal   (Followers: 7)
International Cardiovascular Forum Journal     Open Access  
International Journal of Angiology     Hybrid Journal   (Followers: 2)
International Journal of Cardiology     Hybrid Journal   (Followers: 18)
International Journal of Cardiology Hypertension     Open Access   (Followers: 1)
International Journal of Cardiovascular and Cerebrovascular Disease     Open Access   (Followers: 2)
International Journal of Cardiovascular Imaging     Hybrid Journal   (Followers: 2)
International Journal of Cardiovascular Research     Hybrid Journal   (Followers: 6)
International Journal of Heart Rhythm     Open Access  
International Journal of Hypertension     Open Access   (Followers: 8)
International Journal of Hyperthermia     Open Access  
International Journal of Stroke     Hybrid Journal   (Followers: 32)
International Journal of the Cardiovascular Academy     Open Access  
Interventional Cardiology Clinics     Full-text available via subscription   (Followers: 2)
Interventional Cardiology Review     Open Access  
JACC : Basic to Translational Science     Open Access   (Followers: 5)
JACC : Cardiovascular Imaging     Hybrid Journal   (Followers: 18)
JACC : Cardiovascular Interventions     Hybrid Journal   (Followers: 19)
JACC : Heart Failure     Full-text available via subscription   (Followers: 14)
JAMA Cardiology     Hybrid Journal   (Followers: 30)

        1 2 | Last

Similar Journals
Journal Cover
Cardiovascular Research
Journal Prestige (SJR): 3.002
Citation Impact (citeScore): 5
Number of Followers: 15  
  Hybrid Journal Hybrid journal (It can contain Open Access articles)
ISSN (Print) 0008-6363 - ISSN (Online) 1755-3245
Published by Oxford University Press Homepage  [412 journals]
  • Cardiovascular Research at the frontier of biomedical science
    • Authors: Brown S; Sheikh A, Guzik T.
      Abstract: CardioprotectionCardio-oncologyMetabolismGeneticsNon-coding RNAs
      PubDate: Mon, 18 May 2020 00:00:00 GMT
      DOI: 10.1093/cvr/cvaa119
      Issue No: Vol. 116, No. 7 (2020)
  • Highlights from the first ever virtual American College of Cardiology
           World Congress of Cardiology 2020 (ACC.20/WCC)
    • Authors: M. Leucker T.
      Abstract: American College of CardiologyCardiologyClinical trialsCardiovascular medicineCardiovascular research
      PubDate: Mon, 18 May 2020 00:00:00 GMT
      DOI: 10.1093/cvr/cvaa099
      Issue No: Vol. 116, No. 7 (2020)
  • Ticagrelor monotherapy in patients with diabetes mellitus undergoing
           percutaneous coronary interventions: insights from the TWILIGHT trial
    • Authors: Angiolillo D; Baber U, Mehran R.
      Abstract: TicagrelorDiabetesPercutaneous coronary interventionTWILIGHT
      PubDate: Mon, 18 May 2020 00:00:00 GMT
      DOI: 10.1093/cvr/cvaa120
      Issue No: Vol. 116, No. 7 (2020)
  • Cellular communication in a ‘virtual lab’: going beyond the classical
           ligand-receptor interaction
    • Authors: Gladka M.
      Abstract: Intercellular communicationSingle cellSignalling networkNicheNet
      PubDate: Mon, 18 May 2020 00:00:00 GMT
      DOI: 10.1093/cvr/cvaa076
      Issue No: Vol. 116, No. 7 (2020)
  • Postponement of Frontiers in Cardiovascular Biomedicine (FCVB) 2020 due to
           COVID-19: a look forward to 2021
    • Authors: Ferdinandy P; Koller Á, Weber C, et al.
      PubDate: Thu, 23 Apr 2020 00:00:00 GMT
      DOI: 10.1093/cvr/cvaa108
      Issue No: Vol. 116, No. 7 (2020)
  • Binding of SARS-CoV-2 and angiotensin-converting enzyme 2: clinical
    • Authors: Murray E; Tomaszewski M, Guzik T.
      Abstract: ACE inhibitorSARS-CoV-2COVID-19Hypertension
      PubDate: Fri, 17 Apr 2020 00:00:00 GMT
      DOI: 10.1093/cvr/cvaa096
      Issue No: Vol. 116, No. 7 (2020)
  • Mid-term effects of electronic cigarette use on vascular function and
           oxidative stress
    • Authors: Kourea K; Kostelli G, Ikonomidis I.
      Abstract: Electronic cigarettesVascular functionOxidative stressE-cigarettesSmoking
      PubDate: Thu, 09 Apr 2020 00:00:00 GMT
      DOI: 10.1093/cvr/cvaa095
      Issue No: Vol. 116, No. 7 (2020)
  • Scientists on the Spot: Calcium dynamics in heart function
    • Authors: Meli A; Kranias E.
      Abstract: CalciumArrhythmiaHeart failure PhospholambanHeart function
      PubDate: Mon, 16 Mar 2020 00:00:00 GMT
      DOI: 10.1093/cvr/cvaa031
      Issue No: Vol. 116, No. 7 (2020)
  • CircRNAs in the heart: bricks in Brunelleschi’s Dome
    • Authors: De Majo F; da Costa Martins P.
      Pages: 1240 - 1241
      Abstract: This editorial refers to ‘Circular RNA circRNA_000203 aggravates cardiac hypertrophy via suppressing miR26b-5p and miR-140-3p binding to Gata4' by H. Li et al., pp. 1323–1334.
      PubDate: Fri, 07 Feb 2020 00:00:00 GMT
      DOI: 10.1093/cvr/cvaa020
      Issue No: Vol. 116, No. 7 (2020)
  • Flash-forward: the emergence of angiography-derived fractional flow
           reserve in the catheter laboratory
    • Authors: Wong C; Yong A.
      Pages: 1242 - 1245
      Abstract: This editorial refers to ‘Accuracy of computational pressure-fluid dynamics applied to coronary angiography to derive fractional flow reserve: FLASH FFR’, by J. Li et al., pp. 1349–1356.
      PubDate: Tue, 04 Feb 2020 00:00:00 GMT
      DOI: 10.1093/cvr/cvaa015
      Issue No: Vol. 116, No. 7 (2020)
  • Sex-related differences in the ageing brain: time for precision
    • Authors: Costantino S; Paneni F.
      Pages: 1246 - 1248
      Abstract: This editorial refers to ‘Aging influences cerebrovascular myogenic reactivity and BK channel function in a sex-specific manner’, by J.T. Reed et al., pp. 1372–1385.
      PubDate: Tue, 28 Jan 2020 00:00:00 GMT
      DOI: 10.1093/cvr/cvaa014
      Issue No: Vol. 116, No. 7 (2020)
  • Single nuclei sequencing of entire mammalian hearts: strain-dependent
           cell-type composition and velocity
    • Authors: Wolfien M; Galow A, Müller P, et al.
      Pages: 1249 - 1251
      PubDate: Fri, 03 Apr 2020 00:00:00 GMT
      DOI: 10.1093/cvr/cvaa054
      Issue No: Vol. 116, No. 7 (2020)
  • Blood pressure changes correlate with short-chain fatty acid production
           potential shifts under a synbiotic intervention
    • Authors: Bartolomaeus H; Avery E, Bartolomaeus T, et al.
      Pages: 1252 - 1253
      PubDate: Tue, 31 Mar 2020 00:00:00 GMT
      DOI: 10.1093/cvr/cvaa083
      Issue No: Vol. 116, No. 7 (2020)
  • Corrigendum
    • Pages: 1322 - 1322
      Abstract: Corrigendum to: Moderate but not severe hypothermia causes pro-arrhythmic changes in cardiac electrophysiology [Cardiovasc Res 2020;doi:10.1093/cvr/cvz309]
      PubDate: Fri, 13 Mar 2020 00:00:00 GMT
      DOI: 10.1093/cvr/cvaa048
      Issue No: Vol. 116, No. 7 (2020)
  • Corrigendum
    • Pages: 1334 - 1334
      Abstract: Corrigendum to: Loss of life expectancy from air pollution compared to other risk factors: a worldwide perspective [Cardiovasc Res 2020; doi:10.1093/cvr/cvaa025]
      PubDate: Thu, 09 Apr 2020 00:00:00 GMT
      DOI: 10.1093/cvr/cvaa073
      Issue No: Vol. 116, No. 7 (2020)
  • Corrigendum
    • Pages: 1385 - 1385
      Abstract: Corrigendum: Scientists on the Spot: calcium dynamics in heart function [Cardiovasc Res 2020; doi:10.1093/cvr/cvaa031]
      PubDate: Sun, 26 Apr 2020 00:00:00 GMT
      DOI: 10.1093/cvr/cvaa105
      Issue No: Vol. 116, No. 7 (2020)
  • Changes in high-density lipoprotein microRNA might create a lasting memory
           of high-fat diet
    • Authors: Chamorro-Jorganes A; Anwar M, Emanueli C.
      Pages: 1237 - 1239
      Abstract: This editorial refers to ‘High-density lipoprotein remodelled in hypercholesterolaemic blood induce epigenetically driven down-regulation of endothelial HIF-1α expression in a preclinical animal model’, by S. Ben-Aicha et al., pp. 1288–1299.
      PubDate: Tue, 24 Dec 2019 00:00:00 GMT
      DOI: 10.1093/cvr/cvz334
      Issue No: Vol. 116, No. 7 (2019)
  • Lipoprotein receptor signalling in atherosclerosis
    • Authors: Mineo C.
      Pages: 1254 - 1274
      Abstract: AbstractThe founding member of the lipoprotein receptor family, low-density lipoprotein receptor (LDLR) plays a major role in the atherogenesis through the receptor-mediated endocytosis of LDL particles and regulation of cholesterol homeostasis. Since the discovery of the LDLR, many other structurally and functionally related receptors have been identified, which include low-density lipoprotein receptor-related protein (LRP)1, LRP5, LRP6, very low-density lipoprotein receptor, and apolipoprotein E receptor 2. The scavenger receptor family members, on the other hand, constitute a family of pattern recognition proteins that are structurally diverse and recognize a wide array of ligands, including oxidized LDL. Among these are cluster of differentiation 36, scavenger receptor class B type I and lectin-like oxidized low-density lipoprotein receptor-1. In addition to the initially assigned role as a mediator of the uptake of macromolecules into the cell, a large number of studies in cultured cells and in in vivo animal models have revealed that these lipoprotein receptors participate in signal transduction to modulate cellular functions. This review highlights the signalling pathways by which these receptors influence the process of atherosclerosis development, focusing on their roles in the vascular cells, such as macrophages, endothelial cells, smooth muscle cells, and platelets. Human genetics of the receptors is also discussed to further provide the relevance to cardiovascular disease risks in humans. Further knowledge of the vascular biology of the lipoprotein receptors and their ligands will potentially enhance our ability to harness the mechanism to develop novel prophylactic and therapeutic strategies against cardiovascular diseases.
      PubDate: Fri, 13 Dec 2019 00:00:00 GMT
      DOI: 10.1093/cvr/cvz338
      Issue No: Vol. 116, No. 7 (2019)
  • Myocardial slices come to age: an intermediate complexity in vitro cardiac
           model for translational research
    • Authors: Pitoulis F; Watson S, Perbellini F, et al.
      Pages: 1275 - 1287
      Abstract: AbstractAlthough past decades have witnessed significant reductions in mortality of heart failure together with advances in our understanding of its cellular, molecular, and whole-heart features, a lot of basic cardiac research still fails to translate into clinical practice. In this review we examine myocardial slices, a novel model in the translational arena. Myocardial slices are living ultra-thin sections of heart tissue. Slices maintain the myocardium’s native function (contractility, electrophysiology) and structure (multicellularity, extracellular matrix) and can be prepared from animal and human tissue. The discussion begins with the history and current advances in the model, the different interlaboratory methods of preparation and their potential impact on results. We then contextualize slices’ advantages and limitations by comparing it with other cardiac models. Recently, sophisticated methods have enabled slices to be cultured chronically in vitro while preserving the functional and structural phenotype. This is more timely now than ever where chronic physiologically relevant in vitro platforms for assessment of therapeutic strategies are urgently needed. We interrogate the technological developments that have permitted this, their limitations, and future directions. Finally, we look into the general obstacles faced by the translational field, and how implementation of research systems utilizing slices could help in resolving these.
      PubDate: Mon, 23 Dec 2019 00:00:00 GMT
      DOI: 10.1093/cvr/cvz341
      Issue No: Vol. 116, No. 7 (2019)
  • High-density lipoprotein remodelled in hypercholesterolaemic blood induce
           epigenetically driven down-regulation of endothelial HIF-1α expression in
           a preclinical animal model
    • Authors: Ben-Aicha S; Escate R, Casaní L, et al.
      Pages: 1288 - 1299
      Abstract: AbstractAimsHigh-density lipoproteins (HDLs) are circulating micelles that transport proteins, lipids, and miRNAs. HDL-transported miRNAs (HDL-miRNAs) have lately received attention but their effects on vascular cells are not fully understood. Additionally, whether cardiovascular risk factors affect HDL-miRNAs levels and miRNA transfer to recipient cells remains equally poorly known. Here, we have investigated the changes induced by hypercholesterolaemia on HDL-miRNA levels and its effect on recipient endothelial cells (ECs).Methods and resultsPigs were kept on a high-fat diet (HC; n = 10) or a normocholesterolaemic chow (NC; n = 10) for 10 days reaching cholesterol levels of 321.0 (229.7–378.5) mg/dL and 74.0 (62.5–80.2) mg/dL, respectively. HDL particles were isolated, purified, and quantified. HDL-miRNA profiling (n = 149 miRNAs) of HC- and NC-HDLs was performed by multipanel qPCR. Cell cultures of porcine aortic ECs were used to determine whether HDL-miRNAs were delivered to ECs. Potential target genes modulated by miRNAs were identified by bioinformatics and candidate miRNAs were validated by molecular analysis. In vivo effects in the coronary arteries of normocholesterolaemic swine administered HC- or NC-HDLs were analysed. Among the HDL-miRNAs, four were found in different amounts in HC- and NC-HDL (P < 0.05). miR-126-5p and -3p and miR-30b-5p (2.7×, 1.7×, and 1.3×, respectively) were found in higher levels and miR-103a-3p and miR-let-7g-5p (−1.6×, −1.4×, respectively) in lower levels in HC-HDL. miR-126-5p and -3p were transferred from HC-HDL to EC (2.5×; P < 0.05), but not from NC-HDL, by a SRB1-mediated mechanism. Bioinformatics revealed that HIF1α was the miR-126 target gene with the highest predictive value, which was accordingly found to be markedly reduced in HC-HDL-treated ECs and in miR126 mimic transfected ECs. In vivo validation confirmed that HIF1α was diminished in the coronary endothelial layer of NC pigs administered HC-HDL vs. those administered NC-HDL (P < 0.05).ConclusionHypercholesterolaemia induces changes in the miRNA content of HDL enhancing miR126 and its delivery to ECs with the consequent down-regulation of its target gene HIF1α.
      PubDate: Fri, 30 Aug 2019 00:00:00 GMT
      DOI: 10.1093/cvr/cvz239
      Issue No: Vol. 116, No. 7 (2019)
  • Homeobox B9 integrates bone morphogenic protein 4 with inflammation at
           atheroprone sites
    • Authors: Souilhol C; Gauci I, Feng S, et al.
      Pages: 1300 - 1310
      Abstract: AbstractAimsAtherosclerosis develops near branches and bends of arteries that are exposed to disturbed blood flow which exerts low wall shear stress (WSS). These mechanical conditions alter endothelial cells (EC) by priming them for inflammation and by inducing turnover. Homeobox (Hox) genes are developmental genes involved in the patterning of embryos along their anterior–posterior and proximal–distal axes. Here we identified Hox genes that are regulated by WSS and investigated their functions in adult arteries.Methods and resultsEC were isolated from inner (low WSS) and outer (high WSS) regions of the porcine aorta and the expression of Hox genes was analysed by quantitative real-time PCR. Several Hox genes (HoxA10, HoxB4, HoxB7, HoxB9, HoxD8, HoxD9) were significantly enriched at the low WSS compared to the high WSS region. Similarly, studies of cultured human umbilical vein EC (HUVEC) or porcine aortic EC revealed that the expression of multiple Hox genes (HoxA10, HoxB9, HoxD8, HoxD9) was enhanced under low (4 dyn/cm2) compared to high (13 dyn/cm2) WSS conditions. Gene silencing studies identified Hox genes (HoxB9, HoxD8, HoxD9) that are positive regulators of inflammatory molecule expression in EC exposed to low WSS, and others (HoxB9, HoxB7, HoxB4) that regulated EC turnover. We subsequently focused on HoxB9 because it was strongly up-regulated by low WSS and, uniquely, was a driver of both inflammation and proliferation. At a mechanistic level, we demonstrate using cultured EC and murine models that bone morphogenic protein 4 (BMP4) is an upstream regulator of HoxB9 which elicits inflammation via induction of numerous inflammatory mediators including TNF and downstream NF-κB activation. Moreover, the BMP4-HoxB9-TNF pathway was potentiated by hypercholesterolaemic conditions.ConclusionsLow WSS induces multiple Hox genes that control the activation state and turnover of EC. Notably, low WSS activates a BMP4-HoxB9-TNF signalling pathway to initiate focal arterial inflammation, thereby demonstrating integration of the BMP and Hox systems in vascular pathophysiology.
      PubDate: Thu, 29 Aug 2019 00:00:00 GMT
      DOI: 10.1093/cvr/cvz235
      Issue No: Vol. 116, No. 7 (2019)
  • Cardiac resynchronization therapy reduces expression of
           inflammation-promoting genes related to interleukin-1β in heart failure
    • Authors: Bilchick K; Kothari H, Narayan A, et al.
      Pages: 1311 - 1322
      Abstract: AbstractAimsIn light of recent data regarding inflammatory signalling pathways in cardiovascular disease and the recently demonstrated impact of pharmacologic inhibition of interleukin-1β (IL-1β) in heart failure, the primary aim was to assess the physiologic effects of cardiac resynchronization therapy (CRT) on the expression of systemic inflammatory, immune-modulatory, metabolic, and apoptotic genes in peripheral blood mononuclear cells (PBMCs) of patients with heart failure.Methods and resultsWe used RNA sequencing (RNA-Seq) and reverse transcription quantitative real-time polymerase chain reaction (RT-qPCR) to identify gene expression changes in PBMCs in response to CRT. In total, 27 patients were analysed: 12 with heart failure undergoing CRT, 6 with heart failure undergoing standard implanted cardioverter defibrillators, and 9 with coronary artery disease but not heart failure. In CRT patients (median age 65.5 years, interquartile range 63.0–66.8 years, 33% female), RNA-Seq analysis identified 40 genes, including multiple genes associated with the IL-1β pathway, with significant correlations (false discovery rate < 0.05) with four key CRT response measures. CRT was associated with suppression of PBMC expression of IL-1β (1.80-fold decrease, P = 0.047), FOS proto-oncogene (FOS) (3.25-fold decrease, P = 0.01), dual specificity phosphatase 1 (DUSP1) (2.05-fold decrease, P = 0.001), and early growth response 1 (EGR1) (7.38-fold decrease, P = 0.03), and suppression was greater in responders vs. non-responders (P = 0.03 for IL-1β, P = 0.02 for FOS, P = 0.02 for DUSP1, and P = 0.11 for EGR1). Baseline FOS and DUSP-1 levels were greater in responders vs. non-responders (6.15-fold higher, FOS, P = 0.002; 2.60-fold higher, DUSP1, P = 0.0001). CRT responders but not non-responders showed higher baseline gene expression of FOS (P = 0.04) and DUSP1 (P = 0.06) compared with control patients without heart failure. Baseline serum high-sensitivity C-reactive protein levels were 3.47-fold higher in CRT responders vs. non-responders (P = 0.008).ConclusionTreatment of heart failure with CRT resulted in decreased PBMC expression of genes linked to inflammation. Moreover, CRT responders had higher expression of these inflammatory genes prior to CRT and greater suppression of these genes after CRT compared with non-responders.
      PubDate: Tue, 15 Oct 2019 00:00:00 GMT
      DOI: 10.1093/cvr/cvz232
      Issue No: Vol. 116, No. 7 (2019)
  • Circular RNA circRNA_000203 aggravates cardiac hypertrophy via suppressing
           miR-26b-5p and miR-140-3p binding to Gata4
    • Authors: Li H; Xu J, Fang X, et al.
      Pages: 1323 - 1334
      Abstract: AbstractAimsCircular RNAs (circRNAs) are involved in gene regulation in a variety of physiological and pathological processes. The present study aimed to investigate the effect of circRNA_000203 on cardiac hypertrophy and the potential mechanisms involved.Methods and resultsCircRNA_000203 was found to be up-regulated in the myocardium of Ang-II-infused mice and in the cytoplasma of Ang-II-treated neonatal mouse ventricular cardiomyocytes (NMVCs). Enforced expression of circRNA_000203 enhances cell size and expression of atrial natriuretic peptide and β-myosin heavy chain in NMVCs. In vivo, heart function was impaired and cardiac hypertrophy was aggravated in Ang-II-infused myocardium-specific circRNA_000203 transgenic mice (Tg-circ203). Mechanistically, we found that circRNA_000203 could specifically sponge miR-26b-5p, -140-3p in NMVCs. Further, dual-luciferase reporter assay showed that miR-26b-5p, -140-3p could interact with 3′-UTRs of Gata4 gene, and circRNA_000203 could block the above interactions. In addition, Gata4 expression is transcriptionally inhibited by miR-26b-5p, -140-3p mimic in NMVCs but enhanced by over-expression of circRNA_000203 in vitro and in vivo. Functionally, miR-26b-5p, -140-3p, and Gata4 siRNA, could reverse the hypertrophic growth in Ang-II-induced NMVCs, as well as eliminate the pro-hypertrophic effect of circRNA_000203 in NMVCs. Furthermore, we demonstrated that NF-κB signalling mediates the up-regulation of circRNA_000203 in NMVCs exposed to Ang-II treatment.ConclusionsOur data demonstrated that circRNA_000203 exacerbates cardiac hypertrophy via suppressing miR-26b-5p and miR-140-3p leading to enhanced Gata4 levels.
      PubDate: Fri, 09 Aug 2019 00:00:00 GMT
      DOI: 10.1093/cvr/cvz215
      Issue No: Vol. 116, No. 7 (2019)
  • CGRP derived from cardiac fibroblasts is an endogenous suppressor of
           cardiac fibrosis
    • Authors: Li W; Zhang Z, Li X, et al.
      Pages: 1335 - 1348
      Abstract: AbstractAimsAberrant activation of cardiac fibroblasts leads to cardiac fibrosis, and evolving evidences suggest that endogenous bioactive substances derived from cardiac fibroblasts regulate cardiac fibroblasts activation in an autocrine/paracrine manner. Here we first presented evidence that cardiac fibroblasts can synthesize and secrete calcitonin gene-related peptide (CGRP), therefore, this study aimed to investigate the role of cardiac fibroblasts-derived CGRP in cardiac fibroblasts activation and its regulative mechanism.Methods and resultsThe abundantly expression of CGRP in rat, mouse, and human myocardium allowed us to explore the cellular origin of CGRP, and found that the cardiac CGRP was mainly derived from cardiac fibroblasts. Activating TRPA1 with a specific agonist allyl isothiocyanate promoted the synthesis and secretion of CGRP, as well as intracellular Ca2+. These effects were reversed by TRPA1-specific antagonist HC030031 and Ca2+ chelator BAPTA-AM. TGF-β1 was applied to induce the activation of cardiac fibroblasts, and found that TGF-β1 can increase the mRNA expression and secretion levels of CGRP in cardiac fibroblasts. Either CGRP8–37 (CGRP receptor antagonist) or α-CGRP small interfering RNA (siRNA) aggravated TGF-β1-induced proliferation, differentiation, collagen production, and instigated inflammation in cardiac fibroblasts. Moreover, TGF-β1-induced NF-κB activation including IκBα phosphorylation and p65 nuclear translocation were also promoted by CGRP8–37 and α-CGRP siRNA. NF-κB inhibitor pyrrolidinedithiocarbamate ammonium (PDTC) reversed the effects of CGRP8–37 on NF-κB activation. The promotive effects of CGRP8–37 on TGF-β1-induced activation of cardiac fibroblasts were all reversed by PDTC. Monocrotaline (MCT) induces pulmonary arterial hypertension, progressively leading to right ventricular fibrosis. This model of cardiac fibrosis was developed here to test the potentially beneficial effects of TRPA1 activation in vivo. The non-toxic TRPA1 agonist Cinnamaldehyde (CA) inhibited MCT-induced elevation in right ventricle systolic pressure, RV/LV + S, and right ventricular collagen accumulation, as well as down-regulation of CGRP. CA increased the synthesis and secretion of CGRP, and inhibited TGF-β1-induced activation in cardiac fibroblasts.ConclusionOur data suggested an autocrine role for cardiac fibroblasts-derived CGRP in suppressing activation of cardiac fibroblasts through inhibiting NF-κB activation. Increasing autocrine CGRP by activating TRPA1 can ameliorate cardiac fibrosis. These findings support the notion that CGRP derived from cardiac fibroblasts is an endogenous suppressor of cardiac fibrosis.
      PubDate: Wed, 28 Aug 2019 00:00:00 GMT
      DOI: 10.1093/cvr/cvz234
      Issue No: Vol. 116, No. 7 (2019)
  • Accuracy of computational pressure-fluid dynamics applied to coronary
           angiography to derive fractional flow reserve: FLASH FFR
    • Authors: Li J; Gong Y, Wang W, et al.
      Pages: 1349 - 1356
      Abstract: AbstractAimsConventional fractional flow reserve (FFR) is measured invasively using a coronary guidewire equipped with a pressure sensor. A non-invasive derived FFR would eliminate risk of coronary injury, minimize technical limitations, and potentially increase adoption. We aimed to evaluate the diagnostic performance of a computational pressure-flow dynamics derived FFR (caFFR), applied to coronary angiography, compared to invasive FFR.Methods and resultsThe FLASH FFR study was a prospective, multicentre, single-arm study conducted at six centres in China. Eligible patients had native coronary artery target lesions with visually estimated diameter stenosis of 30–90% and diagnosis of stable or unstable angina pectoris. Using computational pressure-fluid dynamics, in conjunction with thrombolysis in myocardial infarction (TIMI) frame count, applied to coronary angiography, caFFR was measured online in real-time and compared blind to conventional invasive FFR by an independent core laboratory. The primary endpoint was the agreement between caFFR and FFR, with a pre-specified performance goal of 84%. Between June and December 2018, matched caFFR and FFR measurements were performed in 328 coronary arteries. Total operational time for caFFR was 4.54 ± 1.48 min. caFFR was highly correlated to FFR (R = 0.89, P = 0.76) with a mean bias of −0.002 ± 0.049 (95% limits of agreement −0.098 to 0.093). The diagnostic performance of caFFR vs. FFR was diagnostic accuracy 95.7%, sensitivity 90.4%, specificity 98.6%, positive predictive value 97.2%, negative predictive value 95.0%, and area under the receiver operating characteristic curve of 0.979.ConclusionsUsing wire-based FFR as the reference, caFFR has high accuracy, sensitivity, and specificity. caFFR could eliminate the need of a pressure wire, technical error and potentially increase adoption of physiological assessment of coronary artery stenosis severity.Clinical Trial RegistrationURL: Unique Identifier: ChiCTR1800019522.
      PubDate: Wed, 06 Nov 2019 00:00:00 GMT
      DOI: 10.1093/cvr/cvz289
      Issue No: Vol. 116, No. 7 (2019)
  • Specific macrophage populations promote both cardiac scar deposition and
           subsequent resolution in adult zebrafish
    • Authors: Bevan L; Lim Z, Venkatesh B, et al.
      Pages: 1357 - 1371
      Abstract: AbstractAimsA robust inflammatory response to tissue injury is a necessary part of the repair process but the deposition of scar tissue is a direct downstream consequence of this response in many tissues including the heart. Adult zebrafish not only possess the capacity to regenerate lost cardiomyocytes but also to remodel and resolve an extracellular scar within tissues such as the heart, but this scar resolution process remains poorly understood. This study aims to characterize the scarring and inflammatory responses to cardiac damage in adult zebrafish in full and investigate the role of different inflammatory subsets specifically in scarring and scar removal.Methods and resultsUsing stable transgenic lines, whole organ imaging and genetic and pharmacological interventions, we demonstrate that multiple inflammatory cell lineages respond to cardiac injury in adult zebrafish. In particular, macrophage subsets (tnfα+ and tnfα−) play prominent roles with manipulation of different phenotypes suggesting that pro-inflammatory (tnfα+) macrophages promote scar deposition following cardiac injury whereas tnfα− macrophages facilitate scar removal during regeneration. Detailed analysis of these specific macrophage subsets reveals crucial roles for Csf1ra in promoting pro-inflammatory macrophage-mediated scar deposition. Additionally, the multifunctional cytokine Osteopontin (Opn) (spp1) is important for initial scar deposition but also for resolution of the inflammatory response and in late-stage ventricular collagen remodelling.ConclusionsThis study demonstrates the importance of a correctly balanced inflammatory response to facilitate scar deposition during repair but also to allow subsequent scar resolution, and full cardiac regeneration, to occur. We have identified Opn as having both pro-fibrotic but also potentially pro-regenerative roles in the adult zebrafish heart, driving Collagen deposition but also controlling inflammatory cell resolution.
      PubDate: Fri, 16 Aug 2019 00:00:00 GMT
      DOI: 10.1093/cvr/cvz221
      Issue No: Vol. 116, No. 7 (2019)
  • Aging influences cerebrovascular myogenic reactivity and BK channel
           function in a sex-specific manner
    • Authors: Reed J; Pareek T, Sriramula S, et al.
      Pages: 1372 - 1385
      Abstract: AbstractAimsThe myogenic reactivity of the middle cerebral arteries (MCA) protects the brain by altering the diameter in response to changes in lumen pressure. Large conductance potassium (BK) channels are known to regulate the myogenic reactivity, yet, it is not clear how aging alters the myogenic reactivity via the BK channel in males and females. Thus, we hypothesize that age-associated changes in BK channel subunits modulate the myogenic reactivity in a sex-specific manner.Methods and resultsWe used vascular reactivity, patch-clamp, and biochemical methods to measure myogenic reactivity, BK channel function, and expression, respectively in cerebral vessels of adult and aged male and female Sprague Dawley rats. Our results suggest that aging and ovariectomy (OVX) exaggerated the myogenic reactivity of MCA in females but attenuated it in males. Aging induced outward eutrophic remodelling in females but inward hypertrophic remodelling in males. Aging decreased total, Kv, BK channel currents, and spontaneous transient outward currents (STOC) in vascular smooth muscle cells isolated from females, but not in males. Aging increased BKα subunit mRNA and protein both in males and females. However, aging decreased BKβ1 subunit protein and mRNA in females only. In males, BKβ1 mRNA is increased, but protein is decreased. Iberiotoxin-induced MCA constriction is lower in aged females but higher in aged males. Activation of BKα (10 µM NS1619) and BKβ1 (10 µM S-Equol) subunits failed to increase STOCs and were unable to decrease the myogenic reactivity of MCA in aged female but not in aged male rats. OVX decreased, but chronic supplementation of oestradiol restored BK channel expression and function.ConclusionOverall our results suggest that aging or OVX-associated downregulation of the BKβ1 expression and function in females results in exaggerated myogenic reactivity of MCA. However, age-associated increase in BK channel function in males attenuated myogenic reactivity of MCA.
      PubDate: Mon, 18 Nov 2019 00:00:00 GMT
      DOI: 10.1093/cvr/cvz314
      Issue No: Vol. 116, No. 7 (2019)
  • miR-378a influences vascularization in skeletal muscles
    • Authors: Krist B; Podkalicka P, Mucha O, et al.
      Pages: 1386 - 1397
      Abstract: AbstractAimsMicroRNA-378a, highly expressed in skeletal muscles, was demonstrated to affect myoblasts differentiation and to promote tumour angiogenesis. We hypothesized that miR-378a could play a pro-angiogenic role in skeletal muscle and may be involved in regeneration after ischaemic injury in mice.Methods and resultsSilencing of miR-378a in murine C2C12 myoblasts did not affect differentiation but impaired their secretory angiogenic potential towards endothelial cells. miR-378a knockout (miR-378a−/−) in mice resulted in a decreased number of CD31-positive blood vessels and arterioles in gastrocnemius muscle. In addition, diminished endothelial sprouting from miR-378a−/− aortic rings was shown. Interestingly, although fibroblast growth factor 1 (Fgf1) expression was decreased in miR-378a−/− muscles, this growth factor did not mediate the angiogenic effects exerted by miR-378a. In vivo, miR-378a knockout did not affect the revascularization of the ischaemic muscles in both normo- and hyperglycaemic mice subjected to femoral artery ligation (FAL). No difference in regenerating muscle fibres was detected between miR-378a−/− and miR-378+/+ mice. miR-378a expression temporarily declined in ischaemic skeletal muscles of miR-378+/+ mice already on Day 3 after FAL. At the same time, in the plasma, the level of miR-378a-3p was enhanced. Similar elevation of miR-378a-3p was reported in the plasma of patients with intermittent claudication in comparison to healthy donors. Local adeno-associated viral vectors-based miR-378a overexpression was enough to improve the revascularization of the ischaemic limb of wild-type mice on Day 7 after FAL, what was not reported after systemic delivery of vectors. In addition, the number of infiltrating CD45+ cells and macrophages (CD45+ CD11b+ F4/80+ Ly6G−) was higher in the ischaemic muscles of miR-378a−/− mice, suggesting an anti-inflammatory action of miR-378a.ConclusionsData indicate miR-378a role in the pro-angiogenic effect of myoblasts and vascularization of skeletal muscle. After the ischaemic insult, the anti-angiogenic effect of miR-378a deficiency might be compensated by enhanced inflammation.
      PubDate: Tue, 27 Aug 2019 00:00:00 GMT
      DOI: 10.1093/cvr/cvz236
      Issue No: Vol. 116, No. 7 (2019)
School of Mathematical and Computer Sciences
Heriot-Watt University
Edinburgh, EH14 4AS, UK
Tel: +00 44 (0)131 4513762

Your IP address:
Home (Search)
About JournalTOCs
News (blog, publications)
JournalTOCs on Twitter   JournalTOCs on Facebook

JournalTOCs © 2009-