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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.
Han et al. (Wed,) studied this question.
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