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Molecular Research in Cardiovascular Disease
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Molecular Research in Cardiovascular Disease

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: closed (30 April 2021) | Viewed by 35338

Special Issue Editors

Prof. Dr. Maria I. Dorobantu

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Guest Editor
1. Corresponding member of the Romanian Academiy, 125, Calea Victoriei, Sector 1, RO - 010071 Bucharest, Romania
2. Department 4-Cardiothoracic Pathology, University of Medicine and Pharmacy Carol Davila, 8, Eroii Sanitari Bvd., 050474 Bucharest, Romania
Interests: ischemic heart disease; atherosclerosis; molecular mechanisms of acute coronary syndromes; arterial hypertension; hypertensive target organ damage
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Maya Simionescu

E-Mail Website
Guest Editor
Romanian Academy-President of the Section of Biological Sciences, Institute of Cellular Biology and Pathology “N. Simionescu”, Bucharest, Romania
Interests: atherosclerosis, cellular, and molecular mechanisms; endothelium; transport of molecules; microcirculation; patho-biochemistry of diabetes mellitus
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Cardiovascular diseases (CVD) are the leading cause of death worldwide. Atherosclerosis, the dominant driver of CVD, is characterized by a process of chronic inflammation and endothelial dysfunction associated with vessel wall accumulation of oxidized low-density lipoproteins.

In advanced stages, endothelial lesions promote atherosclerotic plaque instability, acute events, and ultimately, plaque rupture.

The molecular and cellular mechanisms underlying various cardiovascular diseases are not completely understood. However, several signaling pathways that induce vascular remodeling are essential in both coronary heart disease and in related pathologies, such as pulmonary artery hypertension, suggesting the existence of common mechanisms in these maladies.

With this Special Issue, we aim to present representative data obtained at the interface between basic science and clinical research on the molecular mechanisms of heart and vascular diseases and the novel biomarkers and molecules that can become specific targets for future therapeutic interventions. In addition, we hope that the papers presented will inspire novel innovative investigations at the bench to bedside intersection.

Prof. Dr. Maria I. Dorobantu
Prof. Dr. Maya Simionescu
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • atherosclerosis
  • cardiovascular disease
  • endothelial cells
  • matrix metalloproteinases
  • biomarkers
  • miRNAs
  • epigenetics

Related Special Issue

Published Papers (11 papers)

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Editorial

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4 pages, 198 KiB  
Editorial
Molecular Research in Cardiovascular Disease
by Maria Dorobantu, Maya Simionescu and Nicoleta-Monica Popa-Fotea
Int. J. Mol. Sci. 2021, 22(13), 7199; https://doi.org/10.3390/ijms22137199 - 4 Jul 2021
Cited by 3 | Viewed by 1944
Abstract
Cardiovascular diseases have attracted our full attention not only because they are the main cause of mortality and morbidity in many countries but also because the therapy for and cure of these maladies are among the major challenges of the medicine in the [...] Read more.
Cardiovascular diseases have attracted our full attention not only because they are the main cause of mortality and morbidity in many countries but also because the therapy for and cure of these maladies are among the major challenges of the medicine in the 21st century [...] Full article
(This article belongs to the Special Issue Molecular Research in Cardiovascular Disease)

Research

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16 pages, 4536 KiB  
Article
Rapid Internalization and Nuclear Translocation of CCL5 and CXCL4 in Endothelial Cells
by Annemiek Dickhout, Dawid M. Kaczor, Alexandra C. A. Heinzmann, Sanne L. N. Brouns, Johan W. M. Heemskerk, Marc A. M. J. van Zandvoort and Rory R. Koenen
Int. J. Mol. Sci. 2021, 22(14), 7332; https://doi.org/10.3390/ijms22147332 - 8 Jul 2021
Cited by 4 | Viewed by 2843
Abstract
The chemokines CCL5 and CXCL4 are deposited by platelets onto endothelial cells, inducing monocyte arrest. Here, the fate of CCL5 and CXCL4 after endothelial deposition was investigated. Human umbilical vein endothelial cells (HUVECs) and EA.hy926 cells were incubated with CCL5 or CXCL4 for [...] Read more.
The chemokines CCL5 and CXCL4 are deposited by platelets onto endothelial cells, inducing monocyte arrest. Here, the fate of CCL5 and CXCL4 after endothelial deposition was investigated. Human umbilical vein endothelial cells (HUVECs) and EA.hy926 cells were incubated with CCL5 or CXCL4 for up to 120 min, and chemokine uptake was analyzed by microscopy and by ELISA. Intracellular calcium signaling was visualized upon chemokine treatment, and monocyte arrest was evaluated under laminar flow. Whereas CXCL4 remained partly on the cell surface, all of the CCL5 was internalized into endothelial cells. Endocytosis of CCL5 and CXCL4 was shown as a rapid and active process that primarily depended on dynamin, clathrin, and G protein-coupled receptors (GPCRs), but not on surface proteoglycans. Intracellular calcium signals were increased after chemokine treatment. Confocal microscopy and ELISA measurements in cell organelle fractions indicated that both chemokines accumulated in the nucleus. Internalization did not affect leukocyte arrest, as pretreatment of chemokines and subsequent washing did not alter monocyte adhesion to endothelial cells. Endothelial cells rapidly and actively internalize CCL5 and CXCL4 by clathrin and dynamin-dependent endocytosis, where the chemokines appear to be directed to the nucleus. These findings expand our knowledge of how chemokines attract leukocytes to sites of inflammation. Full article
(This article belongs to the Special Issue Molecular Research in Cardiovascular Disease)
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19 pages, 1719 KiB  
Article
Dysregulated Expression of Arterial MicroRNAs and Their Target Gene Networks in Temporal Arteries of Treatment-Naïve Patients with Giant Cell Arteritis
by Tadeja Kuret, Katja Lakota, Saša Čučnik, Vesna Jurčič, Oliver Distler, Žiga Rotar, Alojzija Hočevar, Snežna Sodin-Šemrl and Mojca Frank-Bertoncelj
Int. J. Mol. Sci. 2021, 22(12), 6520; https://doi.org/10.3390/ijms22126520 - 17 Jun 2021
Cited by 10 | Viewed by 2363
Abstract
In this study, we explored expression of microRNA (miR), miR-target genes and matrix remodelling molecules in temporal artery biopsies (TABs) from treatment-naïve patients with giant cell arteritis (GCA, n = 41) and integrated these analyses with clinical, laboratory, ultrasound and histological manifestations of [...] Read more.
In this study, we explored expression of microRNA (miR), miR-target genes and matrix remodelling molecules in temporal artery biopsies (TABs) from treatment-naïve patients with giant cell arteritis (GCA, n = 41) and integrated these analyses with clinical, laboratory, ultrasound and histological manifestations of GCA. NonGCA patients (n = 4) served as controls. GCA TABs exhibited deregulated expression of several miRs (miR-21-5p, -145-5p, -146a-5p, -146b-5p, -155-5p, 424-3p, -424-5p, -503-5p), putative miR-target genes (YAP1, PELI1, FGF2, VEGFA, KLF4) and matrix remodelling factors (MMP2, MMP9, TIMP1, TIPM2) with key roles in Toll-like receptor signaling, mechanotransduction and extracellular matrix biology. MiR-424-3p, -503-5p, KLF4, PELI1 and YAP1 were identified as new deregulated molecular factors in GCA TABs. Quantities of miR-146a-5p, YAP1, PELI1, FGF2, TIMP2 and MMP9 were particularly high in histologically positive GCA TABs with occluded temporal artery lumen. MiR-424-5p expression in TABs and the presence of facial or carotid arteritis on ultrasound were associated with vision disturbances in GCA patients. Correlative analysis of miR-mRNA quantities demonstrated a highly interrelated expression network of deregulated miRs and mRNAs in temporal arteries and identified KLF4 as a candidate target gene of deregulated miR-21-5p, -146a-5p and -155-5p network in GCA TABs. Meanwhile, arterial miR and mRNA expression did not correlate with constitutive symptoms and signs of GCA, elevated markers of systemic inflammation nor sonographic characteristics of GCA. Our study provides new insights into GCA pathophysiology and uncovers new candidate biomarkers of vision impairment in GCA. Full article
(This article belongs to the Special Issue Molecular Research in Cardiovascular Disease)
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16 pages, 1923 KiB  
Article
Dual Stem Cell Therapy Improves the Myocardial Recovery Post-Infarction through Reciprocal Modulation of Cell Functions
by Sinziana Popescu, Mihai Bogdan Preda, Catalina Iolanda Marinescu, Maya Simionescu and Alexandrina Burlacu
Int. J. Mol. Sci. 2021, 22(11), 5631; https://doi.org/10.3390/ijms22115631 - 26 May 2021
Cited by 13 | Viewed by 2686
Abstract
Mesenchymal stromal cells (MSC) are promising candidates for regenerative therapy of the infarcted heart. However, poor cell retention within the transplantation site limits their potential. We hypothesized that MSC benefits could be enhanced through a dual-cell approach using jointly endothelial colony forming cells [...] Read more.
Mesenchymal stromal cells (MSC) are promising candidates for regenerative therapy of the infarcted heart. However, poor cell retention within the transplantation site limits their potential. We hypothesized that MSC benefits could be enhanced through a dual-cell approach using jointly endothelial colony forming cells (ECFC) and MSC. To assess this, we comparatively evaluated the effects of the therapy with MSC and ECFC versus MSC-only in a mouse model of myocardial infarction. Heart function was assessed by echocardiography, and the molecular crosstalk between MSC and ECFC was evaluated in vitro through direct or indirect co-culture systems. We found that dual-cell therapy improved cardiac function in terms of ejection fraction and stroke volume. In vitro experiments showed that ECFC augmented MSC effector properties by increasing Connexin 43 and Integrin alpha-5 and the secretion of healing-associated molecules. Moreover, MSC prompted the organization of ECFC into vascular networks. This indicated a reciprocal modulation in the functionality of MSC and ECFC. In conclusion, the crosstalk between MSC and ECFC augments the therapeutic properties of MSC and enhances the angiogenic properties of ECFC. Our data consolidate the dual-cell therapy as a step forward for the development of effective treatments for patients affected by myocardial infarction. Full article
(This article belongs to the Special Issue Molecular Research in Cardiovascular Disease)
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8 pages, 979 KiB  
Communication
miR155 Deficiency Reduces Myofibroblast Density but Fails to Improve Cardiac Function after Myocardial Infarction in Dyslipidemic Mouse Model
by David Schumacher, Adelina Curaj, Sakine Simsekyilmaz, Andreas Schober, Elisa A. Liehn and Sebastian F. Mause
Int. J. Mol. Sci. 2021, 22(11), 5480; https://doi.org/10.3390/ijms22115480 - 22 May 2021
Cited by 6 | Viewed by 2320
Abstract
Myocardial infarction remains the most common cause of heart failure with adverse remodeling. MicroRNA (miR)155 is upregulated following myocardial infarction and represents a relevant regulatory factor for cardiac remodeling by engagement in cardiac inflammation, fibrosis and cardiomyocyte hypertrophy. Here, we investigated the role [...] Read more.
Myocardial infarction remains the most common cause of heart failure with adverse remodeling. MicroRNA (miR)155 is upregulated following myocardial infarction and represents a relevant regulatory factor for cardiac remodeling by engagement in cardiac inflammation, fibrosis and cardiomyocyte hypertrophy. Here, we investigated the role of miR155 in cardiac remodeling and dysfunction following myocardial infarction in a dyslipidemic mouse model. Myocardial infarction was induced in dyslipidemic apolipoprotein E-deficient (ApoE−/−) mice with and without additional miR155 knockout by ligation of the LAD. Four weeks later, echocardiography was performed to assess left ventricular (LV) dimensions and function, and mice were subsequently sacrificed for histological analysis. Echocardiography revealed no difference in LV ejection fractions, LV mass and LV volumes between ApoE−/− and ApoE−/−/miR155−/− mice. Histology confirmed comparable infarction size and unaltered neoangiogenesis in the myocardial scar. Notably, myofibroblast density was significantly decreased in ApoE−/−/miR155−/− mice compared to the control, but no difference was observed for total collagen deposition. Our findings reveal that genetic depletion of miR155 in a dyslipidemic mouse model of myocardial infarction does not reduce infarction size and consecutive heart failure but does decrease myofibroblast density in the post-ischemic scar. Full article
(This article belongs to the Special Issue Molecular Research in Cardiovascular Disease)
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17 pages, 2169 KiB  
Article
Alternative C3 Complement System: Lipids and Atherosclerosis
by Maisa Garcia-Arguinzonis, Elisa Diaz-Riera, Esther Peña, Rafael Escate, Oriol Juan-Babot, Pedro Mata, Lina Badimon and Teresa Padro
Int. J. Mol. Sci. 2021, 22(10), 5122; https://doi.org/10.3390/ijms22105122 - 12 May 2021
Cited by 8 | Viewed by 2972
Abstract
Familial hypercholesterolemia (FH) is increasingly associated with inflammation, a phenotype that persists despite treatment with lipid lowering therapies. The alternative C3 complement system (C3), as a key inflammatory mediator, seems to be involved in the atherosclerotic process; however, the relationship between C3 and [...] Read more.
Familial hypercholesterolemia (FH) is increasingly associated with inflammation, a phenotype that persists despite treatment with lipid lowering therapies. The alternative C3 complement system (C3), as a key inflammatory mediator, seems to be involved in the atherosclerotic process; however, the relationship between C3 and lipids during plaque progression remains unknown. The aim of the study was to investigate by a systems biology approach the role of C3 in relation to lipoprotein levels during atherosclerosis (AT) progression and to gain a better understanding on the effects of C3 products on the phenotype and function of human lipid-loaded vascular smooth muscle cells (VSMCs). By mass spectrometry and differential proteomics, we found the extracellular matrix (ECM) of human aortas to be enriched in active components of the C3 complement system, with a significantly different proteomic signature in AT segments. Thus, C3 products were more abundant in AT-ECM than in macroscopically normal segments. Furthermore, circulating C3 levels were significantly elevated in FH patients with subclinical coronary AT, evidenced by computed tomographic angiography. However, no correlation was identified between circulating C3 levels and the increase in plaque burden, indicating a local regulation of the C3 in AT arteries. In cell culture studies of human VSMCs, we evidenced the expression of C3, C3aR (anaphylatoxin receptor) and the integrin αMβ2 receptor for C3b/iC3b (RT-PCR and Western blot). C3mRNA was up-regulated in lipid-loaded human VSMCs, and C3 protein significantly increased in cell culture supernatants, indicating that the C3 products in the AT-ECM have a local vessel-wall niche. Interestingly, C3a and iC3b (C3 active fragments) have functional effects on VSMCs, significantly reversing the inhibition of VSMC migration induced by aggregated LDL and stimulating cell spreading, organization of F-actin stress fibers and attachment during the adhesion of lipid-loaded human VSMCs. This study, by using a systems biology approach, identified molecular processes involving the C3 complement system in vascular remodeling and in the progression of advanced human atherosclerotic lesions. Full article
(This article belongs to the Special Issue Molecular Research in Cardiovascular Disease)
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Review

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27 pages, 4320 KiB  
Review
Extracellular Vesicles: Versatile Nanomediators, Potential Biomarkers and Therapeutic Agents in Atherosclerosis and COVID-19-Related Thrombosis
by Adriana Georgescu and Maya Simionescu
Int. J. Mol. Sci. 2021, 22(11), 5967; https://doi.org/10.3390/ijms22115967 - 31 May 2021
Cited by 21 | Viewed by 4871
Abstract
Cells convey information among one another. One instrument employed to transmit data and constituents to specific (target) cells is extracellular vesicles (EVs). They originate from a variety of cells (endothelial, immune cells, platelets, mesenchymal stromal cells, etc.), and consequently, their surface characteristics and [...] Read more.
Cells convey information among one another. One instrument employed to transmit data and constituents to specific (target) cells is extracellular vesicles (EVs). They originate from a variety of cells (endothelial, immune cells, platelets, mesenchymal stromal cells, etc.), and consequently, their surface characteristics and cargo vary according to the paternal cell. The cargo could be DNA, mRNA, microRNA, receptors, metabolites, cytoplasmic proteins, or pathological molecules, as a function of which EVs exert different effects upon endocytosis in recipient cells. Recently, EVs have become important participants in a variety of pathologies, including atherogenesis and coronavirus disease 2019 (COVID-19)-associated thrombosis. Herein, we summarize recent advances and some of our own results on the role of EVs in atherosclerotic cardiovascular diseases, and discuss their potential to function as signaling mediators, biomarkers and therapeutic agents. Since COVID-19 patients have a high rate of thrombotic events, a special section of the review is dedicated to the mechanism of thrombosis and the possible therapeutic potential of EVs in COVID-19-related thrombosis. Yet, EV mechanisms and their role in the transfer of information between cells in normal and pathological conditions remain to be explored. Full article
(This article belongs to the Special Issue Molecular Research in Cardiovascular Disease)
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19 pages, 1362 KiB  
Review
MicroRNAs in Acute ST Elevation Myocardial Infarction—A New Tool for Diagnosis and Prognosis: Therapeutic Implications
by Alina Ioana Scărlătescu, Miruna Mihaela Micheu, Nicoleta-Monica Popa-Fotea and Maria Dorobanțu
Int. J. Mol. Sci. 2021, 22(9), 4799; https://doi.org/10.3390/ijms22094799 - 30 Apr 2021
Cited by 22 | Viewed by 3623
Abstract
Despite diagnostic and therapeutic advances, coronary artery disease and especially its extreme manifestation, ST elevation myocardial infarction (STEMI), remain the leading causes of morbidity and mortality worldwide. Early and prompt diagnosis is of great importance regarding the prognosis of STEMI patients. In recent [...] Read more.
Despite diagnostic and therapeutic advances, coronary artery disease and especially its extreme manifestation, ST elevation myocardial infarction (STEMI), remain the leading causes of morbidity and mortality worldwide. Early and prompt diagnosis is of great importance regarding the prognosis of STEMI patients. In recent years, microRNAs (miRNAs) have emerged as promising tools involved in many pathophysiological processes in various fields, including cardiovascular diseases. In acute coronary syndromes (ACS), circulating levels of miRNAs are significantly elevated, as an indicator of cardiac damage, making them a promising marker for early diagnosis of myocardial infarction. They also have prognostic value and great potential as therapeutic targets considering their key function in gene regulation. This review aims to summarize current information about miRNAs and their role as diagnostic, prognostic and therapeutic targets in STEMI patients. Full article
(This article belongs to the Special Issue Molecular Research in Cardiovascular Disease)
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26 pages, 2700 KiB  
Review
Endothelial Extracellular Vesicles: From Keepers of Health to Messengers of Disease
by Allison Mathiesen, Tyree Hamilton, Nigeste Carter, Michael Brown, William McPheat and Anca Dobrian
Int. J. Mol. Sci. 2021, 22(9), 4640; https://doi.org/10.3390/ijms22094640 - 28 Apr 2021
Cited by 33 | Viewed by 3724
Abstract
Endothelium has a rich vesicular network that allows the exchange of macromolecules between blood and parenchymal cells. This feature of endothelial cells, along with their polarized secretory machinery, makes them the second major contributor, after platelets, to the particulate secretome in circulation. Extracellular [...] Read more.
Endothelium has a rich vesicular network that allows the exchange of macromolecules between blood and parenchymal cells. This feature of endothelial cells, along with their polarized secretory machinery, makes them the second major contributor, after platelets, to the particulate secretome in circulation. Extracellular vesicles (EVs) produced by the endothelial cells mirror the remarkable molecular heterogeneity of their parent cells. Cargo molecules carried by EVs were shown to contribute to the physiological functions of endothelium and may support the plasticity and adaptation of endothelial cells in a paracrine manner. Endothelium-derived vesicles can also contribute to the pathogenesis of cardiovascular disease or can serve as prognostic or diagnostic biomarkers. Finally, endothelium-derived EVs can be used as therapeutic tools to target endothelium for drug delivery or target stromal cells via the endothelial cells. In this review we revisit the recent evidence on the heterogeneity and plasticity of endothelial cells and their EVs. We discuss the role of endothelial EVs in the maintenance of vascular homeostasis along with their contributions to endothelial adaptation and dysfunction. Finally, we evaluate the potential of endothelial EVs as disease biomarkers and their leverage as therapeutic tools. Full article
(This article belongs to the Special Issue Molecular Research in Cardiovascular Disease)
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15 pages, 4457 KiB  
Review
Insights into the Functional Role of ADTRP (Androgen-Dependent TFPI-Regulating Protein) in Health and Disease
by Cristina Lupu, Maulin M. Patel and Florea Lupu
Int. J. Mol. Sci. 2021, 22(9), 4451; https://doi.org/10.3390/ijms22094451 - 24 Apr 2021
Cited by 12 | Viewed by 2693
Abstract
The novel protein ADTRP, identified and described by us in 2011, is androgen-inducible and regulates the expression and activity of Tissue Factor Pathway Inhibitor, the major inhibitor of the Tissue Factor-dependent pathway of coagulation on endothelial cells. Single-nucleotide polymorphisms in ADTRP associate with [...] Read more.
The novel protein ADTRP, identified and described by us in 2011, is androgen-inducible and regulates the expression and activity of Tissue Factor Pathway Inhibitor, the major inhibitor of the Tissue Factor-dependent pathway of coagulation on endothelial cells. Single-nucleotide polymorphisms in ADTRP associate with coronary artery disease and myocardial infarction, and deep vein thrombosis/venous thromboembolism. Some athero-protective effects of androgen could exert through up-regulation of ADTRP expression. We discovered a critical role of ADTRP in vascular development and vessel integrity and function, manifested through Wnt signaling-dependent regulation of matrix metalloproteinase-9. ADTRP also hydrolyses fatty acid esters of hydroxy-fatty acids, which have anti-diabetic and anti-inflammatory effects and can control metabolic disorders. Here we summarize and analyze the knowledge on ADTRP and try to decipher its functions in health and disease. Full article
(This article belongs to the Special Issue Molecular Research in Cardiovascular Disease)
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14 pages, 1108 KiB  
Review
Regulatory Light Chains in Cardiac Development and Disease
by Kasturi Markandran, Jane Wenjin Poh, Michael A. Ferenczi and Christine Cheung
Int. J. Mol. Sci. 2021, 22(9), 4351; https://doi.org/10.3390/ijms22094351 - 21 Apr 2021
Cited by 10 | Viewed by 3758
Abstract
The role of regulatory light chains (RLCs) in cardiac muscle function has been elucidated progressively over the past decade. The RLCs are among the earliest expressed markers during cardiogenesis and persist through adulthood. Failing hearts have shown reduced RLC phosphorylation levels and that [...] Read more.
The role of regulatory light chains (RLCs) in cardiac muscle function has been elucidated progressively over the past decade. The RLCs are among the earliest expressed markers during cardiogenesis and persist through adulthood. Failing hearts have shown reduced RLC phosphorylation levels and that restoring baseline levels of RLC phosphorylation is necessary for generating optimal force of muscle contraction. The signalling mechanisms triggering changes in RLC phosphorylation levels during disease progression remain elusive. Uncovering this information may provide insights for better management of heart failure patients. Given the cardiac chamber-specific expression of RLC isoforms, ventricular RLCs have facilitated the identification of mature ventricular cardiomyocytes, opening up possibilities of regenerative medicine. This review consolidates the standing of RLCs in cardiac development and disease and highlights knowledge gaps and potential therapeutic advancements in targeting RLCs. Full article
(This article belongs to the Special Issue Molecular Research in Cardiovascular Disease)
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