July 2020
Vol 6, Issue 28

About The Cover

Cover image expansion

ONLINE COVER More than one million people worldwide suffer from pulmonary fibrosis, a deadly disease in which damage in the lungs creates scar tissue that interferes with the lungs' function. While both environmental (e.g. cigarette smoking) and genetic factors contribute to the development of pulmonary fibrosis, the molecular mechanisms underlying the disease have proven difficult to understand. Due to the diverse cellular makeup of the lungs, single-cell technologies such as single-cell RNA sequencing (scRNA-seq) provide a promising platform for scientists to unravel the lungs' cellular complexity and pinpoint key molecular and cellular changes. Habermann et al. performed scRNA-seq of single-cell suspensions from 20 lungs with pulmonary fibrosis and 10 control lungs without the disease, providing a high-resolution view of the changes that occur in lung cells with pulmonary fibrosis, including a shift in epithelial cell phenotypes. In another study, Adams et al. profiled 312,928 nuclei from 32 lungs with idiopathic pulmonary fibrosis (IPF), 28 smoker and non-smoker control lungs, and 18 lungs with chronic obstructive pulmonary disease (COPD). Both studies identified novel cell types/states including a population of abnormal profibrotic epithelial cells in lungs from patients with pulmonary fibrosis that simultaneously express epithelial, mesenchymal, aging, and developmental markers. [CREDIT: KROPSKI LAN, VANDERBILT UNIVERSITY MEDICAL CENTER]