Lindsay J. Celada

This study shows that mechanical stiffness in fibrotic lungs promotes macrophage apoptosis resistance through metabolic reprogramming, contributing to fibrosis progression.

This paper identifies compartment- and cell-specific molecular programs in preclinical familial pulmonary fibrosis using multi-omic profiling and finds these signatures are partially represented in peripheral blood.

This study shows that inhibiting macropinocytosis reduces fibrotic responses in lung fibroblasts and ameliorates pulmonary fibrosis in mice.

The paper uses single-cell transcriptomics to analyze an IPF cohort, revealing a transcriptional deficit refractory to current treatments and identifying STAT3 as a key regulator in the therapeutic gap.