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Our team combines the work of internationally recognized and established teams that have come together to address the molecular, cellular and physiological mechanisms that lead to heart failure (with a growing focus on diastolic dysfunction) and to use this knowledge base to identify relevant targets to reverse the adverse remodeling process and eventually promote myocardial tissue repair. For this purpose, the team develops approaches to preserve cardiac function with focus on arterial and myocardial stiffness, innovative modeling with iPS-derived cardiomyocytes and stem cell biology.

Team Organisation Scheme 2018

We follow three main research axes:

  • To explore the relationships between arterial / myocardial stiffening and the development of diastolic dysfunction and heart failure
  • To use iPS cells- based 2D and 3D models to investigate cardiomyocytes defective pathways that lead to dysfunction
  • To understand the role of cardiac resident stem cells on pathological cardiac tissue repair, notably fibrotic remodeling


Keywords: heart failure, arterial stiffness, stem cells, iPSC, fibrosis, pharmacology



PARCC_team 07_OK_image réduite2 Micro-poétique -©Iglika Christova 2018


  • Publications

    Anti-integrin α therapy improves cardiac fibrosis after myocardial infarction by blunting cardiac PW1 stromal cells.

    There is currently no therapy to limit the development of cardiac fibrosis and consequent heart failure. We have recently shown that cardiac fibrosis post-myocardial infarction (MI) can be regulated by resident cardiac cells with a fibrogenic signature and identified by the expression of PW1 (Peg3). Here we identify αV-integrin (CD51) as an essential regulator of cardiac PW1 cells fibrogenic behavior. We used transcriptomic and proteomic approaches to identify specific cell-surface markers for cardiac PW1 cells and found that αV-integrin (CD51) was expressed in almost all cardiac PW1 cells (93% ± 1%), predominantly as the αVβ1 complex. αV-integrin is a subunit member of the integrin family of cell adhesion receptors and was found to activate complex of latent transforming growth factor beta (TGFβ at the surface of cardiac PW1 cells. Pharmacological inhibition of αV-integrin reduced the profibrotic action of cardiac PW1CD51 cells and was associated with improved cardiac function and animal survival following MI coupled with a reduced infarct size and fibrotic lesion. These data identify a targetable pathway that regulates cardiac fibrosis in response to an ischemic injury and demonstrate that pharmacological inhibition of αV-integrin could reduce pathological outcomes following cardiac ischemia.

    Scientific reports, July 2020