Cardiovascular diseases including congenital heart defects are the leading cause of mortality. Cardiac diseases result in myocyte deficiency that ultimately leads to congestive heart failure. Despite significant advances, conventional treatments do not correct the defects in myocyte numbers and the prognosis of congestive heart failure remains poor. For this reason, the replacement of lost cardiomyocytes is a primary target of regenerative medicine research.
Although recent studies have uncovered the remarkable regenerative capacity of the newborn mammalian heart, this regenerative potential is lost shortly after birth, strongly supporting the hypothesis that a detailed understanding of developmental mechanisms is essential to identify targets for cardiac repair or regeneration in congenital and acquired heart diseases. Triggering cell cycle re-entry of existing cardiomyocytes together with the stimulation of multipotent cardiac progenitor cells currently represent the most promising approaches for cardiac regeneration over the coming years.
Using a combination of state of the art molecular, developmental, physiological and transgenic approaches our group aims to enhance our knowledge of cardiac development and to contribute to a greater understanding of regulatory steps controlling cardiomyocyte proliferation and progenitor cell fate. Identifying how these process are regulated is thus of crucial importance in regenerative medicine and will inform future cardiac repair strategies.

FFC
AFM-Telethon
ANR


Team's publications

Sturny, R.  et al. 2016

FGF10 is required to promote cardiomyocyte proliferation after myocardial infarction

WOS:000379812500009
Cardiovasc. Res. - issue: - volume: 111 - pages: S3-S3.

Rampersad, SN.  et al. 2016

Adaptive phenotypic modulation of human arterial endothelial cells to fluid shear stress-encoded signals: modulation by phosphodiesterase 4D-VE-cadherin signalling

Although cAMP-signalling regulates numerous functions of vascular endothelial cells (VECs), including their ability to impact vascular resistance in response to changes in blood flow dynamics, few of...
Cell. Signal. - issue: 7 - volume: 28 - pages: 741-748.

Rampersad, SN.  et al. 2016

EPAC1 promotes adaptive responses in human arterial endothelial cells subjected to low levels of laminar fluid shear stress: Implications in flow-related endothelial dysfunction

Blood flow-associated fluid shear stress (FSS) dynamically regulates the endothelium's ability to control arterial structure and function. While arterial endothelial cells (AEC) subjected to high...
Cell. Signal. - issue: 6 - volume: 28 - pages: 606-619.

Smith, PM.  et al. 2016

Leptin influences the excitability of area postrema neurons

The area postrema (AP) is a circumventricular organ with important roles in central autonomic regulation. This medullary structure has been shown to express the leptin receptor and has been suggested...
Am. J. Physiol.-Regul. Integr. Comp. Physiol. - issue: 5 - volume: 310 - pages: R440-R448.

Ahles, A.  et al. 2015

Interhelical Interaction and Receptor Phosphorylation Regulate the Activation Kinetics of Different Human beta(1)-Adrenoceptor Variants

G protein-coupled receptors represent the largest class of drug targets, but genetic variation within G protein-coupled receptors leads to variable drug responses and, thereby, compromises their...
J. Biol. Chem. - issue: 3 - volume: 290 - pages: 1760-1769.

Rochais, F.  et al. 2014

FGF10 promotes regional foetal cardiomyocyte proliferation and adult cardiomyocyte cell-cycle re-entry

Aims Cardiomyocyte proliferation gradually declines during embryogenesis resulting in severely limited regenerative capacities in the adult heart. Understanding the developmental processes controlling...
Cardiovasc. Res. - issue: 3 - volume: 104 - pages: 432-442.

Rochais, F.  et al. 2014

FGF10 regulates regional proliferation in the fetal heart through a FOXO3/p27kip1 pathway and promotes cell cycle reentry of adult cardiomyocytes

WOS:000343730100241
Cardiovasc. Res. - issue: - volume: 103 - pages: .

Maurice, DH.  et al. 2014

Cyclic nucleotide phosphodiesterases (PDEs): coincidence detectors acting to spatially and temporally integrate cyclic nucleotide and non-cyclic nucleotide signals

The cyclic nucleotide second messengers cAMP and cGMP each affect virtually all cellular processes. Although these hydrophilic small molecules readily diffuse throughout cells, it is remarkable that...
Biochem. Soc. Trans. - issue: - volume: 42 - pages: 250-256.

Ahles, A.  et al. 2014

The Arg389Gly polymorphism determines structure and activation kinetics of the human beta(1)-adrenergic receptor

WOS:000359538500093
Naunyn-Schmiedebergs Arch. Pharmacol. - issue: - volume: 387 - pages: S24-S24.

Ahles, A.  et al. 2013

Phosphorylation-dependent receptor memory of the human beta(1)-adrenergic receptor

WOS:000209476400005
Naunyn-Schmiedebergs Arch. Pharmacol. - issue: - volume: 386 - pages: S3-S3.

Zhai, K.  et al. 2012

beta-Adrenergic cAMP Signals Are Predominantly Regulated by Phosphodiesterase Type 4 in Cultured Adult Rat Aortic Smooth Muscle Cells

Background: We investigated the role of cyclic nucleotide phosphodiesterases (PDEs) in the spatiotemporal control of intracellular cAMP concentrations in rat aortic smooth muscle cells (RASMCs)....
PLoS One - issue: 10 - volume: 7 - pages: e47826.

Boon, R.  et al. 2012

A Day in the Life of a Young Investigator

WOS:000306977000005
Circulation - issue: 25 - volume: 125 - pages: F145-F150.

Rochais, F.  et al. 2012

Fgf10 regulates fetal cardiac growth

WOS:000301975800412
Cardiovasc. Res. - issue: - volume: 93 - pages: S97-S97.

Ahles, A.  et al. 2012

The Gly389Arg polymorphism determines the activation kinetics of the human beta(1)-adrenergic receptor

WOS:000300779500007
Naunyn-Schmiedebergs Arch. Pharmacol. - issue: - volume: 385 - pages: 4-4.

Goebel, P.  et al. 2012

Identification of novel targets of beta-adrenergic signaling through phosphoproteomics of the heart in vivo

WOS:000300779500124
Naunyn-Schmiedebergs Arch. Pharmacol. - issue: - volume: 385 - pages: 29-30.