Jeremy B. Katzen

The paper identifies KRT17-Stratifin complex as a protective barrier in dysplastic alveolar basaloid cells during chronic fibrosis, revealing mechanisms of alveolar metaplasia and its functional relevance.

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 identifies lysophosphatidic acid (LPA) as a key bioactive lipid that promotes alveolar type 2 cell progenitor activation via AP-1 transcription factors during lung regeneration.

This study shows that targeting DNA-LNPs to endothelial cells enhances transgene expression magnitude, duration, and specificity in target organs.

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.

This study identifies Stc1-expressing myofibroblasts as a distinct lineage that undergoes apoptosis during neonatal lung development, using genetic tools and single-cell RNA-seq.

This paper identifies that lipid nanoparticle-induced inflammation arises from endosomal membrane damage and proposes strategies to mitigate it through galectin inhibition or ESCRT-recruiting lipids.

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

This study develops lipid nanoparticles co-loaded with anti-inflammatory lipids to reduce inflammation from DNA delivery, enabling prolonged transgene expression.

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