With time, organisms change, and the changes of aging are manifested in multiple processes often described as a slowing down of cellular machinery. These processes of slowed replication and defective cellular recycling are often grouped under the term “senescence,” a word that has its origins in the Latin senescere (“to grow old”). Senescence was first described by Hayflick and Moorhead (6) in 1961 when they observed deterioration of the replicative capacity of fetal lung cells after multiple passages in culture. Since then, many of the features of senescent cells have been described, chiefly that senescent cells have exited the cell cycle and rarely undergo apoptosis (9). In addition, senescent cells have been demonstrated to have both paracrine and autocrine effects on their cellular microenvironment largely through the secretion of chemokines and cytokines that define the senescence-associated secretory phenotype (SASP)(1).

Over the past 50 years, there has been a growing understanding of the molecular mechanisms underlying cellular senescence and an appreciation that cellular senescence may play a role in chronic lung diseases across the lifespan, including bronchopulmonary dysplasia (BPD), asthma, chronic obstructive pulmonary disease (COPD), and idiopathic pulmonary fibrosis (2, 7, 9, 11). Recent work has suggested that targeting the senescent cell population through senolytic therapy may provide a therapeutic strategy that would prevent or reverse these chronic lung diseases (5). Understanding the precise mechanisms whereby senescent cells contribute to chronic lung disease and how to target these mechanisms is an active area of scientific inquiry.