Telomerase gene therapy represents a novel effective treatment for pulmonary fibrosis associated with short telomeres by improving pulmonary function, decreasing inflammation and accelerating fiber disappearance in fibrotic lungs.

Alveolar type 2 stem cells are actively maintained by Hippo signaling and Taz promotes alveolar epithelial regeneration and the resolution of bleomycin induced pulmonary fibrosis upon inactivation of the Hippo pathway in Alveolar type 2 stem cells.

It is safe to transplant autologous P63+ progenitor cells isolated from healthy bronchi to IPF patients for the treatment of IPF, and preliminary efficacy has been demonstrated in some patients.

Inhibition of a single fibroblast-associated transcription factor, namely Paired-related Homeobox Protein 1 (PRRX1), is sufficient to dampen lung fibrogenesis.

Nanoscale changes to individual collagen fibrils drive lung fibrosis.

A systemic feature of idiopathic pulmonary fibrosis whereby urine-derived exosomes contain pro-fibrotic microRNAs and interfere with response to tissue injury.

Telomere dysfunction in iPSC-derived type II alveolar epithelial cells causes senescence and gene expression changes including Wnt-related changes that GSK3 inhibition can rescue, providing insight into pulmonary fibrosis pathogenesis.

A meta-analysis of single-cell data reveals an advanced and conserved polarisation state of SPP1⁺ macrophages in multiple human fibrotic tissues.

The synergy between aging and injury impairs alveolar progenitor functions leading to progressive lung fibrosis.