L. Raposo Rodríguez

The paper identifies inflammatory fibroblasts that promote lung repair by enhancing epithelial proliferation through BMP signaling, validated across multiple models and human disease.

This study compares the maturation pathways of wild-type and disease-associated SP-C mutants, showing divergent trafficking and processing due to mutations.

This study shows that regulatory T cells (Tregs) protect against pulmonary fibrosis in a mouse model by reducing fibrosis and promoting tissue repair through immune-mesenchymal-epithelial signaling.

The paper identifies impaired AMPK signaling in AT2 cells as a driver of pulmonary fibrosis and shows restoring AMPK alleviates fibrosis in vivo.

The paper identifies an injury-induced tissue niche (iTCH) in the lung that coordinates regenerative and disease responses through mesenchymal plasticity and signaling pathways.

This study identifies aberrant transitional alveolar epithelial cells in a mouse fibrosis model and shows they activate fibroblasts through a profibrotic secretome.

This study shows that disrupting PGF2α receptor signaling reduces fibrosis in a mouse model of IPF by altering fibroblast dynamics and reducing fibrotic endpoints.

This study uses patient-derived hydrogels to show IPF fibroblasts exhibit increased inflammation and altered contractility in 3D culture compared to 2D.