Single-cell transcriptomics reveals predominantly inflammatory endothelial cell responses and suppressed vascular repair in silicosis
Year: 2025
Type: article
Abstract: Introduction: Silicosis is a progressive fibrotic lung disease without effective treatment options, and its pathogenesis remains incompletely understood, particularly the role of endothelial cells (ECs). Methods: Here, we utilized single-cell RNA sequencing to characterize endothelial responses in lungs from silica-exposed mice. Results: We identified two functionally distinct endothelial subpopulations: 1. An inflammatory EC subtype, exhibiting significantly increased abundance and characterized by high expression of neutrophil-recruiting factors such as Spp1 (osteopontin), CCL (C-C motif chemokine ligand), and ESAM (endothelial cell-selective adhesion molecule), suggesting active involvement in neutrophil influx and persistent inflammation. 2. A reparative EC subtype, marked by upregulation of angiogenesis and vascular repair pathways, which exhibited decreased abundance and functional suppression within the silicotic lung microenvironment. Discussion: These results indicate a pathological shift toward inflammation-amplifying endothelial cells and impaired reparative capacity during silicosis progression. Our findings provide new mechanistic insights into endothelial cell dysfunction in silicosis and highlight potential targets for therapeutic intervention.
Source: Frontiers in Immunology
Authors: Dongli Cao, Huashun Cui, Zequan Chen, Heyang Li, Bing Li, Jianhua Wang
Language: English
Subfield: Pulmonary and Respiratory Medicine
Field: Medicine
Domain: Health Sciences
Open Access status: gold
Estimated APC paid: $3,801
OpenAlex ID: W4413962222
