Jichao Chen

The paper shows that inhibiting apoptosis of alveolar myofibroblasts (AMFs) reprograms them into ductal myofibroblasts (DMFs) in a mouse model, suggesting fate plasticity in lung mesenchymal cells.

LungChat is a conversational multi-agent AI system that integrates multi-omics analysis and biomedical discovery, identifying potential therapeutics for pulmonary diseases.

This study introduces BIGraph-ST, a method that integrates pathway activity and histological features to improve spatial domain identification in spatial transcriptomics, showing better performance in cancer tissues.

The paper identifies AP-1 transcription factors as regulators of a transitional state in lung alveolar type 2 cells during injury-repair, linking chromatin changes to both regeneration and tumorigenesis.

SPPIDER-seq predicts protein-protein interaction sites by considering partner-specific context, outperforming AlphaFold3 on disordered interfaces and revealing partner-specific patterns in TP53 interactions.

This study generates region-specific airway basal stem cells from human pluripotent stem cells by modulating the NOGGIN-BMP axis, showing distinct differentiation potentials for proximal and distal airway cell types.

The paper identifies morphogenic, molecular, and cellular adaptations in the chicken lung that enable unidirectional airflow through developmental processes and a novel alveolar cell type.

This study shows that CEBPA restricts alveolar type 2 cell plasticity in mice, with loss of CEBPA allowing reactivation of a progenitor program in neonatal cells and increased plasticity in mature cells after injury.

The paper shows that deleting p53 in endothelial cells during hyperoxia generates transitional endothelial cells, improving lung development and reversing vascular damage in BPD.

The paper introduces an inducible tricolor reporter mouse for simultaneous imaging of lysosomes, mitochondria, and microtubules in native tissues at single-cell resolution.

This study investigates sex-dependent molecular and cellular changes in mouse lungs exposed to hyperoxia, identifying distinct progenitor and reparative responses in males and females.

This study shows that alveolar type 1 cells play an intermediary role in lung epithelial repair during Sendai virus infection by persisting in AT2-cell-depleted areas and interacting with immune cells.

The paper classifies mouse lung mesenchymal cells into three axes using single-cell RNA-seq and imaging, identifying two myofibroblast populations with distinct markers and developmental fates.

The paper shows NKX2-1 uses differential chromatin binding to resolve opposing cell fates in mouse lung progenitors, with YAP/TAZ loss altering its binding sites and leading to transcriptional changes.

The paper introduces a quantitative method to construct ligand-receptor interactomes from scRNA-seq data and applies it to mouse lungs infected with Sendai virus.

The paper investigates the functional redundancy and additivity of four Lef/Tcf transcription factors in lung epithelial progenitors using genetic knockout models in mice.

The paper analyzes single-cell RNA-seq data to identify ACE2 expression patterns in human lung epithelial cells, finding high ACE2 expression in alveolar type II cells and co-expression with pathogen receptors.

The paper shows that Vegfa from alveolar type 1 cells specifies a distinct endothelial population in the mouse lung, marked by Car4 and involved in alveologenesis.