A study led by researchers at Tsinghua University in Beijing has elicited the mechanism whereby the protein leucine-rich repeat kinase 2 prevents alveolar type II epithelial cell dysfunction, limiting profibrotic responses during progression of pulmonary fibrosis.

A Chinese study has established a previously unknown direct mechanistic link between elevated mechanical tension caused by impaired alveolar regeneration and progressive idiopathic pulmonary fibrosis (IPF), highlighting a pathogenic mechanism that may underlie fibrosis.