Summary
Abstract Telomere dysfunction has emerged as a primary contributor to diseases within the human lung. Over the past five years, our group has shown that telomere dysfunction limits the proliferative capacity of lung epithelial cells and renders the lung susceptible to injury. In addition, we have found that the senescent lung epithelium secrets a number of bioactive proteins that have unexpected roles in physiology and lung repair. Here we extend our findings to test the centrality of the type II alveolar epithelial cell (AEC2). We build on previous studies that have investigated the roll of A
