Arnaud Mailleux
  • E-mail :[email]
  • Phone : 0157277584
  • Location : Paris, France
Last update 2017-11-07 10:33:33.986

Arnaud Mailleux PhD - Lung Fibrosis / Fibroblast Biology Research

Course and current status

2000-2004       Ph.D. training (Pierre and Marie Curie University), Curie Institute, CNRS / UMR 144, Dr. Jean Paul Thiery lab, supervision: Dr. Saverio Bellusci, Paris, France.

“Roles of the FGF10/FGFR2b signaling pathway in lung and mammary gland ontogeny”.


2004-2008       Research fellow in Cell Biology (Post Doc.), Harvard Medical School, Dept. of Cell Biology; Pr Joan Brugge lab (chair person), Boston, MA, USA.

“Using mouse models to define the role of cell death in mammary gland development and breast cancer initiation“ and “Regulation of apoptosis in mammary epithelial cells upon matrix detachment.”


2008-2013       Research Supervisor (CR2 INSERM) at the French National Institute for Health and Medical Research (INSERM), Unit 700 « Physiopathology and Epidemiology of respiratory Insufficiency » (Dr M. Pretolani), team #3 “Lung inflammation and fibrogenesis” (Prof. B Crestani), Paris France.


2013-               Research Supervisor (CR1 INSERM) at the French National Institute for Health and Medical Research (INSERM), Unit 1152 (since 01/2014, ex U700) “ Physiopathology and Epidemiology of respiratory diseases “(Dr M. Pretolani), team #3 “Lung inflammation and fibrogenesis” (Prof. B Crestani), Paris France.

“Reactivation of developmental signaling pathways in lung fibrosis: from patients to mouse models.”

Scientific summary

Adult respiratory diseases are a major burden in terms of morbidity and mortality and, particularly as related to chronic respiratory disease, are of increasing concern. Our disease model is Idiopathic Pulmonary Fibrosis (IPF), a rare chronic fibrotic pulmonary disease of unknown etiology, which results in the progressive destruction of lung. Median survival after diagnosis is 3 years. According to the current paradigm, IPF results from progressive alterations of alveolar epithelial cells leading to the recruitment of mesenchymal cells to the alveolar regions of the lung with secondary deposition of extracellular matrix, and destruction of the normal lung structure and physiology. IPF develops in a susceptible individual, and is promoted by interaction with environmental agents such as inhaled particles, tobacco smoke, inhaled pollutants, viral and bacterial agents. Genetic susceptibility is probably central to the pathophysiology of IPF. Aging is both a susceptibility marker and a major driver of the disease, through mechanisms that are not yet fully elucidated. Two drugs are currently available for the treatment of pulmonary fibrosis: pirfenidone, a small molecule which probable targets lung fibroblasts through multiple mechanisms, and nintedanib, an inhibitor of tyrosine kinases.

The anarchic epithelial repair observed in IPF is accompanied by reactivation of signaling pathways involved in fetal lung development. Thus, our research team is focused on elucidating the mechanisms and the consequences of the reactivation of developmental signaling pathways during lung fibrosis, and identifying new therapeutic targets.

SCIENTIFIC expertise: Lung development and fibrogenesis, fibroblast biology, mammary gland biology (ontogenesis and oncogenesis), cell death (apoptosis and other cell death programs) and cell signaling (in particular FGF and Hedgehog signalling pathways).

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