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  1. Article ; Online: Prostaglandins bet on regulatory T cells to promote therapeutic revascularization.

    Silvestre, Jean-Sébastien

    Cardiovascular research

    2023  Volume 119, Issue 5, Page(s) 1097–1099

    MeSH term(s) Humans ; T-Lymphocytes, Regulatory ; Dinoprostone ; Prostaglandin-E Synthases ; Prostaglandins ; Th1 Cells ; Ischemia
    Chemical Substances Dinoprostone (K7Q1JQR04M) ; Prostaglandin-E Synthases (EC 5.3.99.3) ; Prostaglandins
    Language English
    Publishing date 2023-04-25
    Publishing country England
    Document type Editorial ; Comment
    ZDB-ID 80340-6
    ISSN 1755-3245 ; 0008-6363
    ISSN (online) 1755-3245
    ISSN 0008-6363
    DOI 10.1093/cvr/cvad051
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Modeling Acute Pericarditis: An Inflammatory Step Toward Tailored Therapeutic Strategies.

    Silvestre, Jean-Sébastien

    JACC. Basic to translational science

    2021  Volume 6, Issue 2, Page(s) 151–153

    Language English
    Publishing date 2021-02-22
    Publishing country United States
    Document type Editorial ; Comment
    ISSN 2452-302X
    ISSN (online) 2452-302X
    DOI 10.1016/j.jacbts.2020.12.005
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: CCL21 in Acute Coronary Syndromes: Biomarker of the 21st Century?

    Silvestre, Jean-Sébastien

    Journal of the American College of Cardiology

    2019  Volume 74, Issue 6, Page(s) 783–785

    MeSH term(s) Acute Coronary Syndrome ; Angina, Unstable ; Biomarkers ; Chemokine CCL21 ; Chemokines ; Humans ; Prognosis
    Chemical Substances Biomarkers ; CCL21 protein, human ; Chemokine CCL21 ; Chemokines
    Language English
    Publishing date 2019-08-07
    Publishing country United States
    Document type Editorial ; Comment
    ZDB-ID 605507-2
    ISSN 1558-3597 ; 0735-1097
    ISSN (online) 1558-3597
    ISSN 0735-1097
    DOI 10.1016/j.jacc.2019.06.029
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.MO 196: Show issues

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  4. Article: Editorial: Inflammation and Reparative Process After Cardiac Injury.

    Silvestre, Jean-Sébastien / Mallat, Ziad

    Frontiers in cardiovascular medicine

    2019  Volume 6, Page(s) 162

    Language English
    Publishing date 2019-11-08
    Publishing country Switzerland
    Document type Editorial
    ZDB-ID 2781496-8
    ISSN 2297-055X
    ISSN 2297-055X
    DOI 10.3389/fcvm.2019.00162
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: Rôle délétère des lymphocytes B de la zone marginale de la rate dans le remodelage ventriculaire après un infarctus du myocarde.

    Duval, Vincent / Alayrac, Paul / Mallat, Ziad / Silvestre, Jean-Sébastien

    Medecine sciences : M/S

    2022  Volume 38, Issue 10, Page(s) 766–768

    Title translation Deleterious role of spleen marginal zone B lymphocytes in ventricular remodeling after myocardial infarction.
    MeSH term(s) B-Lymphocytes ; Humans ; Myocardial Infarction ; Spleen ; Ventricular Remodeling
    Language French
    Publishing date 2022-10-11
    Publishing country France
    Document type News
    ZDB-ID 632733-3
    ISSN 1958-5381 ; 0767-0974
    ISSN (online) 1958-5381
    ISSN 0767-0974
    DOI 10.1051/medsci/2022119
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  6. Article: Emerging Roles of the Atypical Chemokine Receptor 3 (ACKR3) in Cardiovascular Diseases.

    Duval, Vincent / Alayrac, Paul / Silvestre, Jean-Sébastien / Levoye, Angélique

    Frontiers in endocrinology

    2022  Volume 13, Page(s) 906586

    Abstract: Chemokines, and their receptors play a crucial role in the pathophysiology of cardiovascular diseases (CVD). Chemokines classically mediate their effects by binding to G-protein-coupled receptors. The discovery that chemokines can also bind to atypical ... ...

    Abstract Chemokines, and their receptors play a crucial role in the pathophysiology of cardiovascular diseases (CVD). Chemokines classically mediate their effects by binding to G-protein-coupled receptors. The discovery that chemokines can also bind to atypical chemokine receptors (ACKRs) and initiate alternative signaling pathways has changed the paradigm regarding chemokine-related functions. Among these ACKRs, several studies have highlighted the exclusive role of ACKR3, previously known as C-X-C chemokine receptor type 7 (CXCR7), in CVD. Indeed, ACKR3 exert atheroprotective, cardioprotective and anti-thrombotic effects through a wide range of cells including endothelial cells, platelets, inflammatory cells, fibroblasts, vascular smooth muscle cells and cardiomyocytes. ACKR3 functions as a scavenger receptor notably for the pleiotropic chemokine CXCL12, but also as a activator of different pathways such as β-arrestin-mediated signaling or modulator of CXCR4 signaling through the formation of ACKR3-CXCR4 heterodimers. Hence, a better understanding of the precise roles of ACKR3 may pave the way towards the development of novel and improved therapeutic strategies for CVD. Here, we summarize the structural determinant characteristic of ACKR3, the molecules targeting this receptor and signaling pathways modulated by ACKR3. Finally, we present and discuss recent findings regarding the role of ACKR3 in CVD.
    MeSH term(s) Cardiovascular Diseases/genetics ; Chemokine CXCL12 ; Endothelial Cells/metabolism ; Humans ; Receptors, CXCR/metabolism ; Signal Transduction/physiology
    Chemical Substances ACKR3 protein, human ; Chemokine CXCL12 ; Receptors, CXCR
    Language English
    Publishing date 2022-06-29
    Publishing country Switzerland
    Document type Journal Article ; Review ; Research Support, Non-U.S. Gov't
    ZDB-ID 2592084-4
    ISSN 1664-2392
    ISSN 1664-2392
    DOI 10.3389/fendo.2022.906586
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  7. Article ; Online: When the vessels use their brain for therapeutic revascularization.

    Silvestre, Jean-Sébastien

    Arteriosclerosis, thrombosis, and vascular biology

    2014  Volume 34, Issue 2, Page(s) 237–238

    MeSH term(s) Animals ; Diabetic Foot/surgery ; Humans ; Ischemia/surgery ; Muscle, Skeletal/blood supply ; Neovascularization, Physiologic ; Neural Stem Cells/transplantation
    Language English
    Publishing date 2014-02
    Publishing country United States
    Document type Comment ; Editorial
    ZDB-ID 1221433-4
    ISSN 1524-4636 ; 1079-5642
    ISSN (online) 1524-4636
    ISSN 1079-5642
    DOI 10.1161/ATVBAHA.113.302845
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 1705: Show issues Location:
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  8. Article ; Online: MRP-14 Preach the Worse for Platelets and Monocytes Union in Peripheral Artery Disease.

    Annex, Brian H / Silvestre, Jean-Sébastien

    Journal of the American College of Cardiology

    2018  Volume 71, Issue 1, Page(s) 66–68

    MeSH term(s) Blood Platelets ; Humans ; Monocytes ; P-Selectin ; Peripheral Arterial Disease ; Platelet Activation
    Chemical Substances P-Selectin
    Language English
    Publishing date 2018-01-05
    Publishing country United States
    Document type Editorial ; Comment
    ZDB-ID 605507-2
    ISSN 1558-3597 ; 0735-1097
    ISSN (online) 1558-3597
    ISSN 0735-1097
    DOI 10.1016/j.jacc.2017.11.023
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    Zs.MO 196: Show issues

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  9. Article ; Online: Fréquence cardiaque - Quand les macrophages battent la mesure.

    Silvestre, Jean-Sébastien / Vandecasteele, Grégoire

    Medecine sciences : M/S

    2018  Volume 34, Issue 10, Page(s) 820–823

    Abstract: Macrophages regulate cardiac homeostasis under pathological and physiological conditions. Recent studies have elegantly substantiated the presence of specific subset of macrophages residing within the distal atrioventricular node in mice and humans. ... ...

    Title translation Heart rate: when macrophages hit the note.
    Abstract Macrophages regulate cardiac homeostasis under pathological and physiological conditions. Recent studies have elegantly substantiated the presence of specific subset of macrophages residing within the distal atrioventricular node in mice and humans. These macrophages directly couple with cardiomyocytes via connexin-43-containing gap junctions and increase atrioventricular conduction by accelerating cardiomyocyte repolarization. Conditional deletion of connexin-43 in macrophages or congenital lack of macrophages delay nodal conduction and foster progressive atrioventricular block. Exhaustive understanding of the role of tissue-resident macrophages in normal and aberrant cardiac conduction could initiate the development of therapeutic strategies focused on the modulation of macrophage functions in heart arrhythmia.
    MeSH term(s) Animals ; Arrhythmias, Cardiac/etiology ; Arrhythmias, Cardiac/pathology ; Arrhythmias, Cardiac/therapy ; Cardiac Conduction System Disease/etiology ; Cardiac Conduction System Disease/pathology ; Heart Rate/physiology ; Humans ; Macrophages/pathology ; Macrophages/physiology ; Mice ; Myocytes, Cardiac/physiology ; Myocytes, Cardiac/ultrastructure
    Language French
    Publishing date 2018-11-19
    Publishing country France
    Document type Journal Article ; Review
    ZDB-ID 632733-3
    ISSN 1958-5381 ; 0767-0974
    ISSN (online) 1958-5381
    ISSN 0767-0974
    DOI 10.1051/medsci/2018207
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  10. Article ; Online: Vascular endothelial growth factor and angiogenesis: the XBP1 games.

    Silvestre, Jean-Sébastien

    Circulation

    2013  Volume 127, Issue 16, Page(s) 1644–1646

    MeSH term(s) Animals ; Endoplasmic Reticulum Stress/drug effects ; Humans ; Vascular Endothelial Growth Factor A/pharmacology ; Vascular Endothelial Growth Factor Receptor-2/agonists
    Chemical Substances VEGFA protein, human ; Vascular Endothelial Growth Factor A ; vascular endothelial growth factor A, mouse ; Vascular Endothelial Growth Factor Receptor-2 (EC 2.7.10.1)
    Language English
    Publishing date 2013-04-23
    Publishing country United States
    Document type Comment ; Editorial
    ZDB-ID 80099-5
    ISSN 1524-4539 ; 0009-7322 ; 0069-4193 ; 0065-8499
    ISSN (online) 1524-4539
    ISSN 0009-7322 ; 0069-4193 ; 0065-8499
    DOI 10.1161/CIRCULATIONAHA.113.002336
    Database MEDical Literature Analysis and Retrieval System OnLINE

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