Chronic obstructive pulmonary disease (COPD) is a common lung disease characterized by persistent airflow obstruction and a gradual worsening of symptoms, particularly in the context of bacterial and viral infections during COPD exacerbations (1). Although this disease is often associated with cigarette smoking, exposure to a wide range of noxious inhaled particulates, including air pollution and biomass combustion products, is now understood to contribute to COPD development in genetically and/or physiologically susceptible individuals (1). COPD pathology is characterized by chronic inflammation of the airways, which, in the long term, leads to structural changes to the affected organs, i.e., small airway fibrosis, emphysema, and remodeling of the pulmonary vasculature. Ultimately, changes in the pulmonary vasculature can lead to pulmonary hypertension, cardiac hypertrophy, and myocardial fibrosis (1).

Dr. Jazmin Calyeca chats with authors selected for the outstanding abstract presentation award

Until recently, our understanding of human lung development has been extremely limited, as most studies in the field are extrapolated from animal models, primarily rodents. Several recent findings have demonstrated stark cellular and molecular differences between rodent and human lung (1), emphasizing the important need for studies in human samples. Given the challenges associated with obtaining and using prenatal human tissues to investigate developmental processes, the techniques and approaches for analysis have been very limiting. Several technological advances, such as single-cell and single-nucleus RNA sequencing (RNA-seq) and spatial transcriptomics allow scientists to leverage the availability of human tissues. Single-nucleus sequencing can exploit previously frozen archival tissues to provide opportunities to optimize studies.