CV Science

Arnaud Mailleux PhD - Lung Fibrosis / Fibroblast Biology Research

Course and current status

Training and diplomas:

2000-2004       Ph.D. training in Developmental Biology (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.”

2018 Professorial thesis (HDR), Paris Diderot University

"Reactivation of Developmental Signalling pathways in Idiopathic Pulmonary Fibrosis." 

2023 University degree (DU) in "Creation, analysis, and valorization of omics biological data"

Position:

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-  2024       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.”

2025 -     Research Director (DR2  INSERM) at INSERM U1149 "Research Center on Inflammation" (Pr. V. Paradis). Co-leader with Pr Crestani of Team iFi "Inflammation and fibrosis in respiratory diseases »

Other:

2018- 2021         Secretary of Group 03.01 "Molecular Pathology and Functional Genomics"  of European Respiratory Society (ERS)  Assembly 3

2022- 2024         Head of Group 03.01 "Molecular Pathology and Functional Genomics"  of European Respiratory Society (ERS)  Assembly 3

2025 - 2028       Secretary of ERS  Assembly 3 "Basic and Translational Sciences".

Member of the Scientific Committee of RespiFIL (Rare Respiratory Diseases Healthcare Network – OrphaLung)

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.

Our project aims to elucidate the mechanisms involved in the development of pulmonary fibrosis (PF) and identify new therapeutic targets. As mentionned above, we are focusing primarily on idiopathic pulmonary fibrosis (IPF), while also using PF associated with rheumatoid arthritis (RA) and systemic scleroderma (SSc), as models of autoimmune PF. Over the past decade, our team's main areas of research have focused on the reactivation of developmental pathways, the control of abnormal fibroblast phenotype and the genetics of pulmonary fibrosis. We are now expanding our efforts in two new directions: 1) identifying the immune and inflammatory components of PF, and 2) understanding the development of lung cancer in the context of PF.
Our team brings together a wide range of scientists (developmental and cell biology, immunology) and clinical researchers (adult pulmonologists, geneticists, immunologists and pathologists).

Our research focuses on the pathophysiology of fibrosing diseases, tumor development, inflammation and immunology of the lung.

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