Dakota L. Jones

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.

This study shows disease-associated mutations can directionally alter epigenetic age in iPSC-derived organoids, providing a model to study aging and disease interactions.

This study shows that mechanical-nuclear signaling in alveolar fibroblasts influences lung regeneration by modulating transcriptional identity and epithelial repair after injury.

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

The paper establishes a human iPSC-derived co-culture model of pulmonary fibrosis that reveals bidirectional fibrogenic epithelial-mesenchymal crosstalk and identifies potential druggable pathways.

This study shows that transient nuclear softening with TSA treatment enhances cell migration and matrix formation in porcine meniscal cells, with full restoration of transcriptional phenotype and function within 7 days.

This study identifies YAP and TAZ as regulators of periosteal expansion during fracture repair, showing their role in cell proliferation and BMP4 regulation.

This study shows that alveolar epithelial type I cells propagate mechanical signals that affect lung homeostasis and disease states through intercellular communication.

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