José Luis De La Pompa (0000-0001-6761-7265)

Personal information

Biography

José Luis de la Pompa holds an MSc (Biology) from the Universidad Complutense (Madrid, 1985) and a PhD (Genetics) from the Universidad Autónoma (Madrid, 1990). During his postdoc with T. W. Mak at the Ontario Cancer Institute and Amgen Institute (Toronto, Canada), he mastered the techniques of mouse genetic manipulation. His work in this period contributed to the understanding of the role of tumor suppressor genes and different signaling pathways in the regulation of cell proliferation, differentiation, and patterning during mouse development. He became interested in cardiac development after generating and characterizing an NFATc1 mutant with severely defective cardiac valve morphogenesis, and this work led him to the study of the role of Notch signaling pathway in cardiac development. He subsequently held positions as group leader at the EMBL (Monterotondo, Rome, Italy) and Associate Professor at the CADB (Rochester, NY, USA).

José Luis returned to Spain in 2001 to head the Molecular Oncology Department at the Institut de Recerca Oncologica in Barcelona, where his group pioneered the study of the role of Notch in cardiac valve formation. In 2004 he moved to the Centro Nacional de Biotecnología (CNB) in Madrid, where his group continued the study of the role of Notch in the heart, publishing important papers in the field. In 2006 he extended his research to the role of Notch in adult heart homeostasis and opened a new research line in zebrafish heart and fin regeneration. He joined the CNIC in 2009.

Activities

Collapse all

Fundación Centro Nacional de Investigaciones Cardiovasculares Carlos III: Madrid, ES

2009 to present | Intercellular signaling in cardiovascular development and disease (Intercellular signaling in cardiovascular development and disease)

Employment

José Luis De La Pompa

https://orcid.org/0000-0001-6761-7265

Personal information

Websites & social links

Other IDs

Biography

Activities

Employment (1)

Fundación Centro Nacional de Investigaciones Cardiovasculares Carlos III: Madrid, ES

Education and qualifications (2)

Universidad Autonoma de Madrid Facultad de Ciencias: Madrid, Madrid, ES

Universidad Complutense de Madrid: Madrid, Comunidad de Madrid, ES

Professional activities (1)

European Society of Cardiology: Sophia Antipolis, FR

Works (50 of 117)

Tunneling through cardiac jelly

Cardiac electrical abnormalities in a mouse model of left ventricular non-compaction cardiomyopathy

Beyond genomic studies of congenital heart defects through systematic modelling and phenotyping

Deficient GATA6–CXCR7 signaling leads to bicuspid aortic valve

Intricate MIB1-NOTCH-GATA6 Interactions in Cardiac Valvular and Septal Development

Deficient GATA6-ACKR3/CXCR7 signaling leads to bicuspid aortic valve

Cooperative Response to Endocardial Notch Reveals Interaction With Hippo Pathway

Nrg1 Regulates Cardiomyocyte Migration and Cell Cycle in Ventricular Development

Novel Association of the NOTCH Pathway Regulator MIB1 Gene With the Development of Bicuspid Aortic Valve

A cooperative response to endocardial NOTCH signaling stimulation regulates transcriptional activity during cardiac valve development and disease

Don’t Break the Axis: Placental Inflammation Leads to Congenital Heart Disease

Origin of congenital coronary arterio-ventricular fistulae from anomalous epicardial and myocardial development

A Human Hereditary Cardiomyopathy Shares a Genetic Substrate With Bicuspid Aortic Valve

Beta-3 adrenergic receptor overexpression reverses aortic stenosis–induced heart failure and restores balanced mitochondrial dynamics

Neuregulin-1 regulates cardiomyocyte dynamics, cell cycle progression, and maturation during ventricular chamber morphogenesis

En Face Endocardial Cushion Preparation for Planar Morphogenesis Analysis in Mouse Embryos

Adhesion G protein–coupled receptor Gpr126/Adgrg6 is essential for placental development

DACH1-Driven Arterialization: Angiogenic Therapy for Ischemic Heart Disease?

Heterotopic ossification in mice overexpressing Bmp2 in Tie2+ lineages

Midkine-a regulates the formation of a fibrotic scar during zebrafish heart regeneration

Midkine-a regulates the formation of a fibrotic scar during zebrafish heart regeneration

Identification of a peripheral blood gene signature predicting aortic valve calcification.

Association Between Left Ventricular Noncompaction and Vigorous Physical Activity.

Trabeculated Myocardium in Hypertrophic Cardiomyopathy: Clinical Consequences

Fibrous caps in atherosclerosis form by Notch-dependent mechanisms common to arterial media development

Notch and Bmp signaling pathways act coordinately during the formation of the proepicardium.

Loss of Caveolin-1 and caveolae leads to increased cardiac cell stiffness and functional decline of the adult zebrafish heart.

Loss of Caveolin-1 and caveolae leads to increased cardiac cell stiffness and functional decline of the adult zebrafish heart

Human pre-valvular endocardial cells derived from pluripotent stem cells recapitulate cardiac pathophysiological valvulogenesis

Coronary arterial development is regulated by a Dll4-Jag1-EphrinB2 signaling cascade

NOTCH activation promotes valve formation by regulating the endocardial secretome

Actin dynamics and the Bmp pathway drive apical extrusion of proepicardial cells

Myocardial Notch1-Rbpj deletion does not affect NOTCH signaling, heart development or function

Notch and interacting signalling pathways in cardiac development, disease, and regeneration

Dynamic regulation of Notch1 activation and Notch ligand expression in human thymus development

Bmp2 and Notch cooperate to pattern the embryonic endocardium

A novel source of arterial valve cells linked to bicuspid aortic valve without raphe in mice

Control of cardiac jelly dynamics by NOTCH1 and NRG1 defines the building plan for trabeculation

Myocardial Bmp2 gain causes ectopic EMT and promotes cardiomyocyte proliferation and immaturity

Deletion of Fstl1 (Follistatin-Like 1) From the Endocardial/Endothelial Lineage Causes Mitral Valve Disease

Mesenchymal Stem Cell Migration and Proliferation Are Mediated by Hypoxia-Inducible Factor-1α Upstream of Notch and SUMO Pathways.

Marginal zone B cells control the response of follicular helper T cells to a high-cholesterol diet.

Notch signalling restricts inflammation and serpine1 in the dynamic endocardium of the regenerating zebrafish heart.

Endothelial Jag1-RBPJ signalling promotes inflammatory leukocyte recruitment and atherosclerosis.

Notch signalling in ventricular chamber development & cardiomyopathy.

Sequential Ligand-Dependent Notch Signaling Activation Regulates Valve Primordium Formation and Morphogenesis.

The Chromatin Remodeling Complex Chd4/NuRD Controls Striated Muscle Identity and Metabolic Homeostasis.

Morphogenesis of myocardial trabeculae in the mouse embryo.

Congenital coronary artery anomalies: a bridge from embryology to anatomy and pathophysiology-a position statement of the development, anatomy, and pathology ESC Working Group.

Endocardial Notch Signaling in Cardiac Development and Disease.

Peer review (14 reviews for 6 publications/grants)