Aging affects reprogramming of pulmonary capillary endothelial cells after lung injury in male mice

M Marin Truchi M Marine Gautier-Isola G Grégoire Savary C Célia Scribe A Arun Lingampally H Hugo Cadis A Alberto Baeri V Virginie Magnone (Université Côte d'Azur, CNRS, INSERM, Institut de Pharmacologie Moléculaire et Cellulaire) C Cédric Girard-Riboulleau M Marie-Jeanne Arguel C Clémentine de Schutter J Julien Fassy N Nihad Boukrout R Romain Larrue N Nathalie Martin R Roger Rezzonico O Olivier Pluquet M Michael Perrais V Véronique Hofman C Charles-Hugo Marquette P Paul Hofman A Andreas Günther N Nicolas Ricard (Biosanté unit U1292, Grenoble Alpes University, INSERM, CEA) P Pascal Barbry (Université Côte d'Azur, CNRS, INSERM, Institut de Pharmacologie Moléculaire et Cellulaire) S Sylvie Leroy K Kevin Lebrigand (Université Côte d'Azur, CNRS, INSERM, Institut de Pharmacologie Moléculaire et Cellulaire) S Saverio Bellusci C Christelle Cauffiez G Georges Vassaux N Nicolas Pottier B Bernard Mari

Abstract

Abstract Aging increases the risk of developing fibrotic diseases by hampering tissue regeneration after injury. Using longitudinal single-cell RNA-seq and spatial transcriptomics, here we compare the transcriptome of bleomycin (BLM) -induced fibrotic lungs of young and aged male mice, at 3 time points corresponding to the peak of fibrosis, regeneration, and resolution. We find that lung injury shifts the transcriptomic profiles of three pulmonary capillary endothelial cells (PCEC) subpopulations. The associated signatures are linked to pro-angiogenic signaling with strong Lrg1 expression and do not progress similarly throughout the resolution process between young and old animals. Moreover, part of this set of resolution-associated markers is also detected in PCEC from samples of patients with idiopathic pulmonary fibrosis. Finally, we find that aging also alters the transcriptome of PCEC, which displays typical pro-fibrotic and pro-inflammatory features. We propose that age-associated alterations in specific PCEC subpopulations may interfere with the process of lung progenitor differentiation, thus contributing to the persistent fibrotic process typical of human pathology.

Article Details

Volume / Issue Vol. 16, Issue 1
Published August 06, 2025
ISSN 2041-1723
Publisher Nature Portfolio

Journal Info

Nature Communications

Nature Portfolio

ISSN: 2041-1723 Open Access Life Sciences

Authors (31)

M

Marin Truchi

M

Marine Gautier-Isola

G

Grégoire Savary

C

Célia Scribe

A

Arun Lingampally

H

Hugo Cadis

A

Alberto Baeri

V

Virginie Magnone

Université Côte d'Azur, CNRS, INSERM, Institut de Pharmacologie Moléculaire et Cellulaire

C

Cédric Girard-Riboulleau

M

Marie-Jeanne Arguel

C

Clémentine de Schutter

J

Julien Fassy

N

Nihad Boukrout

R

Romain Larrue

N

Nathalie Martin

R

Roger Rezzonico

O

Olivier Pluquet

M

Michael Perrais

V

Véronique Hofman

C

Charles-Hugo Marquette

P

Paul Hofman

A

Andreas Günther

N

Nicolas Ricard

Biosanté unit U1292, Grenoble Alpes University, INSERM, CEA

P

Pascal Barbry

Université Côte d'Azur, CNRS, INSERM, Institut de Pharmacologie Moléculaire et Cellulaire

S

Sylvie Leroy

K

Kevin Lebrigand

Université Côte d'Azur, CNRS, INSERM, Institut de Pharmacologie Moléculaire et Cellulaire

S

Saverio Bellusci

C

Christelle Cauffiez

G

Georges Vassaux

N

Nicolas Pottier

B

Bernard Mari