Understanding myofibroblast origin in the fibrotic lung.

Idiopathic pulmonary fibrosis (IPF) is characterized by accumulation of myofibroblasts (MYFs) and extracellular matrix components, which leads to severe distortion and scarring of the gas exchange units of the lung, the alveoli, and ultimately respiratory failure. Fibrosis-associated MYFs are therefore widely regarded as the culprits that compromise the architectural makeup of the lung in fibrotic disease. During the past decade, the cellular source of MYFs has been intensely investigated.

Senescence of lung mesenchymal stem cells of preterm infants by cyclic stretch and hyperoxia via p21.

Phenotype distortion of lung resident mesenchymal stem cells (MSC) in preterm infants is a hallmark event in the pathogenesis of bronchopulmonary dysplasia (BPD). Here, we evaluated the impact of cyclic mechanical stretch (CMS) and hyperoxia (HOX). The negative action of HOX on proliferation and cell death was more pronounced at 80% than at 40%.

Anti-CCL2 therapy reduces oxygen toxicity to the immature lung.

Oxygen toxicity constitutes a key contributor to bronchopulmonary dysplasia (BPD). Critical step in the pathogenesis of BPD is the inflammatory response in the immature lung with the release of pro-inflammatory cytokines and the influx of innate immune cells. Identification of efficient therapies to alleviate the inflammatory response remains an unmet research priority.