Bin Liu

This study shows that loss of PKN2 leads to fibroblast reprogramming and ECM remodelling in pulmonary fibrosis by altering key pathways and secretion.

This study shows that an AKAP13 genetic variant promotes fibrosis by altering epithelial signaling, and inhibiting AKAP13's RhoGEF activity reduces fibrotic markers in IPF models.

The paper uses spatial multiomic profiling to identify distinct fibrotic epithelial niches in IPF, revealing a KRT5low/KRT17 epithelial population and its association with SPP1 macrophages.

The paper identifies rare pathogenic variants associated with pulmonary fibrosis by analyzing whole genome sequencing data and linking them to cytoskeletal dysfunction.

This study develops a compact prime editor with reduced reverse transcriptase activity, showing efficient editing and enabling flexible split-PE design for in vivo delivery.