Actualités: Publication IPMC/Nature Communications/Dr. Bernard Mari/Equipe B. Mari_G.Vassaux

Présentation

A study published in Nature Communications, conducted in collaboration with the University of Lille (Canther, ONCOLille) and Justus Liebig University Giessen (Germany), shows that aging reduces the lung’s ability to repair itself after injury, which is often the cause of many lung diseases, including idiopathic pulmonary fibrosis.

https://pmc.ncbi.nlm.nih.gov/articles/PMC12328796/pdf/41467_2025_Article_62431.pdf

The defect associated with aging stems in part from “capillary endothelial cells,” which are present in the lungs and essential for both gas exchange and blood vessel remodeling. These cells have the ability to change their identity and function, a characteristic known as “plasticity.” The team’s hypothesis is that this plasticity gives them the ability to regenerate damaged tissue. By combining several methods (single-cell sequencing and spatial transcriptomics), we mapped the identity changes of these cells in young and old mice in a model of pulmonary fibrosis.

The results show that these capillary cells lose their ability to reprogram themselves with age and are less effective at activating the mechanisms that enable them to regenerate. This work identifies promising molecular targets, offering new prospects for stimulating lung regeneration in older people and counteracting these fibrotic phenomena.

https://ihu-respirera.fr/fr/vieillissement-reparation-poumon