MATHIAS MERICSKAY
  • E-mail :[email]
  • Phone : 0146835325
  • Location : Châtenay-Malabry, France
Last update 2017-09-18 16:12:57.84

MATHIAS MERICSKAY PhD Molecular and Cellular Developmental Biology

Course and current status

Current position : CR1 INSERM RESEARCHER at INSERM UMR-S 1180

Signalling and Cardiovascular Pathophysiology

(Director AM Gomez, co-director R. Fischmeister)

University Paris-Sud 11, Faculty of Pharmacy, Châtenay-Malabry, France.

Previous positions:

2014-2016: Co-head of Genetics and physiopathology of muscle tissues group, INSERM U1164 - UMR CNRS 8256 Biology of Adaptation and Aging, University Pierre et Marie Curie Paris 6

2009-13: CR1 INSERM, University Pierre et Marie Curie Paris 6, UR4 Aging, Stress and Inflammation Department

2007:CR1 INSERM nomination, University Pierre et Marie Curie Paris 6, CNRS UMR 7079 Physiology and Physiopathology Department

2003-07: CR2 INSERM investigator, University Pierre et Marie Curie Paris 6, CNRS UMR 7079 Physiology

2000-03: Post-doctoral fellow, Department of Biochemistry and Molecular Biology, Mount Sinai School of Medecine, New York, USA. Group of Prof. David Sassoon. Role of of Wnt morphogens

1995-1999: PhD, Laboratory of Molecular and Cellular Differentiation, Institut Pasteur and University Paris 7. Dir: Pr Denise Paulin. Regulation and Function of Desmin gene during the development of the cardiovascular and skeletal muscle systems in the mouse

Scientific summary

My research focuses on the molecular mechanisms involved in the structural and
metabolic remodeling underlying the pathogenesis of heart failure. I study the
role of SRF as a key regulator of cardiac genes that is repressed in different
models of cardiomyopathies and in human heart failure. Our group showed that
SRF is playing a key role for the maintenance of cardiac, visceral and arterial
smooth muscle contractility and endothelial cells angiogenesis. SRF co-regulates
genes encoding contractile proteins, notably all actin isoform, integrins and VEGF
signaling as well as energy metabolism and microRNAs. These results point to a
central role of SRF in the coupling of structure and energy metabolism, a
cornerstone for muscle tissues functions that is altered in genetic diseases like
dilated cardiomyoapthy and during ageing. More recently I identified defects in
NAD coenzyme metabolism in the failing heart of SRF Heart-KO mice and in
human failing hearts. My ongoing research program aims to restore NAD
homeostasis as a new therapeutic approach to cure heart failure.

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