News
Seminar

Ana Pardo-Saganta, PhD

Professor Lung Inflammation and Repair

Institute for Lung Health - Justus Liebig University

German Center for Lung Research, GIESSEN (Germany)

"Coordinated healing: heterotypic cellular interactions in lung injury and repair"

host : A. MARAVER (IRCM)

Chronic lung disease such as IPF or COPD develops over extended periods of time and are
characterized by failure in mechanisms of repair (1,2). Both pathologies are considered age-related
diseases exhibiting most of the hallmarks of aging including stem cell exhaustion and altered
intercellular communication (3). In the last years, novel epithelial progenitor cells have been identified
and demonstrated to contribute to lung repair. In fact, distinct subpopulations of alveolar type (AT) 2
cells have been shown to have higher regenerative capacity (4-8). Recent findings shed light to the
mechanisms of regeneration of the alveolar epithelium (8-11); however, a better understanding of the
coordinated processes of tissue repair from different stem cell pools after injury is crucial to restore
the delicate lung architecture. Our research focuses on the study of the interplay between these
epithelial progenitor populations and neighboring cell types of their microenvironment in the
development of lung disease.
It is now generally accepted that epithelial cell loss or dysfunction drives the development of lung
fibrosis (12-15). We have identified an additional function for AT2 cells that in addition to serve as
adult stem cells of the alveolar epithelium can play a profibrotic role directly activating adjacent
fibroblast. This communication is mediated by the Notch pathway and their blockade seems to
attenuate the fibrotic phenotype, revealing a potential therapy for IPF, a fatal disease with no cure, a
median survival of 3-5 years post-diagnosis and whose incidence in increasing in the last years (1).
Thus, our findings support the notion that the pathophysiology of pulmonary fibrosis relies in part, on
the Notch-regulated interaction between aberrant cellular populations of the fibrotic lung and that
unravelling this complex microenvironment is critical to find efficient treatments for IPF.
References
1. Schneider JL, et al. The aging lung: physiology, disease and immunity. Cell. 2021 Apr
15;184(8):1990-2019. doi: 10.1016/j.cell.2021.03.005.
2. Han S, et al. Alveolar epithelial regeneration in the aging lung. .J Clin Invest. 2023 Oct
16;133(20):e170504. doi: 10.1172/JCI170504
3. Lopez-Otin C. et al. Hallmarks of aging: An expanding universe. Cell 2023, Jan 19;186(2):243-278.
doi: 10.1016/j.cell.2022.11.001
4. Zacharias WJ. et al, Nature 2018 Mar 8;555(7695):251-255. doi: 10.1038/nature25786.
5. Nabhan AN. et al., Science 2018 Mar 9;359(6380):1118-1123. doi: 10.1126/science.aam6603
6. Chen et al., Am J Physiol Lung Cell Mol Physiol. 2017 Jul 1;313(1):L41-L51. doi:
10.1152/ajplung.00564.2016.
7. Ahmadvand N. et al., Eur Respir J. 2021 Nov 4;58(5):2004168. doi: 10.1183/13993003.04168-
2020.
8. Choi J. et al., Cell Stem Cell 2020 Sep 3;27(3):366-382.e7. doi: 10.1016/j.stem.2020.06.020.
9. Kobayashi Y. et al, Nat Cell Biol 2020 Aug;22(8):934-946. doi: 10.1038/s41556-020-0542-8.
10. Strunz M. et al., Nat Comm 2020. Jul 16;11(1):3559. doi: 10.1038/s41467-020-17358-3.
11. Jiang P. et al., Am J Respir Crit Care Med. 2020 Jun 1;201(11):1443-1447. doi:
10.1164/rccm.201909-1726LE.
12. Sakai, N. & Tager, A. M. Fibrosis of two: Epithelial cell-fibroblast interactions in pulmonary
fibrosis. Biochim. Biophys. Acta - Mol. Basis Dis. 1832, 911–921 (2013).
13. Barkauskas, C. E. & Noble, P. W. Cellular Mechanisms of Tissue Fibrosis. 7. New insights into the
cellular mechanisms of pulmonary fibrosis. AJP Cell Physiol. 306, C987–C996 (2014).
14. Xie T. et al. Abnormal respiratory progenitors in fibrotic lung injury. Stem Cell Res Ther.;13(1):64
(2022).
15. Konkimalla A, et al. Lung Regeneration: Cells, Models, and Mechanisms. Cold Spring Harb
Perspect Biol.; a040873 (2021).

Professor Jifang Zhou, MD, PhD, MPH  & Dr. Yue Zhai, MD, PhD,  (Lecturer)

School of International Business, China Pharmaceutical University (CPU), China

"Reimbursement of Anticancer Drugs in Asia and France: A Comparative Analysis of Health Technology Assessment Frameworks and Real-World Evidence

This presentation offers a comparative overview of drug reimbursement policies for anticancer therapies across Asia and France, with a particular focus on oncology. Drawing on large-scale health insurance databases and electronic health record (EHR) systems, our team examines how reimbursement criteria and pharmaceutical benefits are shaped by real-world evidence, including safety profiles and treatment efficacy observed in patient cohorts. We aim to highlight key similarities and differences across health systems, and to discuss implications for policy and clinical practice

host: Prof E. DESHAYES (ICM)

Pierre Lemieux

Vincent LOUBIERE, PhD

Institut de Génétique Humaine (IGH), UMR 9002

CNRS - Université de Montpellier

"Decoding Persistent Gene Networks in Epigenetic Cancer models"

host : E. JULIEN(IRCM)

Daniel MUNOZ-ESPIN, PhD

CRUK Cambridge Centre Early Detection Programme, 

Hutchison/MRC Research Centre; Cambridge University

"Aging, senescence and reprogramming in lung cancer: therapeutic interventions"

host: A. Maraver (IRCM)

David PEPIN, PhD

Harvard Medical School - Massachusetts General Hospital (USA)

"Role of Cancer associated Mesothelial cells in Tumor Microenvironment"

hôte : Nathalie Bonnefoy & Maeva Chauvin (IRCM)

Pr. David Pépin, Ph.D., is an Associate Professor of Surgery at Harvard Medical School and Massachusetts General Hospital. He trained as a molecular and developmental biologist, earning his doctorate at the University of Ottawa and completing postdoctoral training in reproductive biology and ovarian cancer research at MGH. His laboratory is focused on women’s health, from fertility to ovarian cancer. His team has pioneered research on the role of developmental hormone signals, such as anti?Müllerian hormone (AMH), in regulating the tumor microenvironment through stromal cells such as cancer?associated mesothelial cells (CAMCs). Pr. Pépin’s work combines advanced preclinical models and biological insights to uncover novel therapeutic targets for ovarian cancer and women’s health, bridging basic science with clinical applications.