WNT-dependent interaction between inflammatory fibroblasts and FOLR2+ macrophages promotes fibrosis in chronic kidney disease - Université Paris Cité Accéder directement au contenu
Article Dans Une Revue Nature Communications Année : 2024

WNT-dependent interaction between inflammatory fibroblasts and FOLR2+ macrophages promotes fibrosis in chronic kidney disease

Renaud Leclere
Anne Vincent-Salomon
Sean Eddy
Wenjun Ju

Résumé

Chronic kidney disease (CKD) is a public health problem driven by myofibroblast accumulation, leading to interstitial fibrosis. Heterogeneity is a recently recognized characteristic in kidney fibroblasts in CKD, but the role of different populations is still unclear. Here, we characterize a proinflammatory fibroblast population (named CXCL-iFibro), which corresponds to an early state of myofibroblast differentiation in CKD. We demonstrate that CXCL-iFibro co-localize with macrophages in the kidney and participate in their attraction, accumulation, and switch into FOLR2+ macrophages from early CKD stages on. In vitro, macrophages promote the switch of CXCL-iFibro into ECM-secreting myofibroblasts through a WNT/β-catenin-dependent pathway, thereby suggesting a reciprocal crosstalk between these populations of fibroblasts and macrophages. Finally, the detection of CXCL-iFibro at early stages of CKD is predictive of poor patient prognosis, which shows that the CXCL-iFibro population is an early player in CKD progression and demonstrates the clinical relevance of our findings.
Fichier principal
Vignette du fichier
s41467-024-44886-z.pdf (8.08 Mo) Télécharger le fichier
Origine Fichiers éditeurs autorisés sur une archive ouverte
Licence

Dates et versions

hal-04592846 , version 1 (29-05-2024)

Licence

Identifiants

Citer

Camille Cohen, Rana Mhaidly, Hugo Croizer, Yann Kieffer, Renaud Leclere, et al.. WNT-dependent interaction between inflammatory fibroblasts and FOLR2+ macrophages promotes fibrosis in chronic kidney disease. Nature Communications, 2024, 15 (1), pp.743. ⟨10.1038/s41467-024-44886-z⟩. ⟨hal-04592846⟩
8 Consultations
5 Téléchargements

Altmetric

Partager

Gmail Mastodon Facebook X LinkedIn More