Loss of senescent cells improves pulmonary function in mice

Most cells can divide only a limited number of times and eventually undergo permanent cell cycle arrest, a state known as cellular senescence. Cellular senescence is mediated by activation of specific cellular signaling pathways involving the proteins p19^ARF and p16^INK4A. Precise control of cell cycle arrest and senescence are important for a number of biological processes, including embryonic development, wound healing, and tissue regeneration. Accumulating evidence also indicates that cellular senescence contributes to tissue aging.

In this issue of JCI Insight, Masataka Sugimoto and colleagues at the Juntendo University School of Medicine in Tokyo examined the role of cellular senescence in aging lungs, as there is a well-documented decrease in lung function with age. Using transgenic mice in which they could selectively eliminate cells that express p19^ARF, Sugimoto and colleagues demonstrate that the loss of senescent cells improved lung function in mice. Further studies will be required to determine exactly how senescent cells impair lung function.