Arvind Konkimalla1,2, Aleksandra Tata1 and Purushothama Rao Tata1,3,4,5 1Department of Cell Biology, Duke University School of Medicine, Durham, North Carolina 27710, USA 2Medical Scientist Training Program, Duke University School of Medicine, Durham, North Carolina 27710, USA 3Duke Cancer Institute, Duke University School of Medicine, Durham, North Carolina 27710, USA 4Center for Advanced Genomic Technologies, Duke University, Durham, North Carolina 27710, USA 5Duke Regeneration Center, Duke University School of Medicine, Durham, North Carolina 27710, USA Correspondence: purushothamarao.tataduke.edu

Lung epithelium, the lining that covers the inner surface of the respiratory tract, is directly exposed to the environment and thus susceptible to airborne toxins, irritants, and pathogen-induced damages. In adult mammalian lungs, epithelial cells are generally quiescent but can respond rapidly to repair of damaged tissues. Evidence from experimental injury models in rodents and human clinical samples has led to the identification of these regenerative cells, as well as pathological metaplastic states specifically associated with different forms of damages. Here, we provide a compendium of cells and cell states that exist during homeostasis in normal lungs and the lineage relationships between them. Additionally, we discuss various experimental injury models currently being used to probe the cellular sources—both resident and recruited—that contribute to repair, regeneration, and remodeling following acute and chronic injuries. Finally, we discuss certain maladaptive regeneration-associated cell states and their role in disease pathogenesis.