Advances in cellular senescence in idiopathic pulmonary fibrosis (Review)

Idiopathic pulmonary fibrosis (IPF) is a progressive, irreversible and fatal interstitial lung disease of unknown cause, with a median survival of 2-3 years. Its pathogenesis is unclear and there is currently no effective treatment for IPF. Approximately two-thirds of patients with IPF are >60 years old, with a mean age of 66 years, suggesting a link between aging and IPF. However, the mechanism by which aging promotes development of PF remains unclear. Senescence of alveolar epithelial cells and lung fibroblasts (LFs) and their senescence-associated secretion phenotype (SASP) may be involved in the occurrence and development of IPF. The present review focus on senescence of LFs and epithelial and stem cells, as well as SASP, the activation of profibrotic signaling pathways and potential treatments for pathogenesis of IPF.

Automated summary

Idiopathic pulmonary fibrosis (IPF) is a progressive, irreversible and fatal interstitial lung disease of unknown cause, with a median survival of 2-3 years. Aging may be linked to the development of IPF, but the mechanism remains unclear. Senescence of alveolar epithelial cells and lung fibroblasts (LFs) and their senescence-associated secretion phenotype (SASP) may play a role in IPF. This review focuses on the senescence of LFs and epithelial and stem cells, SASP, profibrotic signaling pathway activation, and potential treatments for IPF pathogenesis.