The Role of p53‐Mediated Cellular Senescence in Idiopathic Pulmonary Fibrosis

An increasing body of evidence suggests that cellular senescence is a risk factor for the development of idiopathic pulmonary fibrosis (IPF). Cellular senescence is a permanent state by which cells cease to divide and adopt an irreversible cell cycle arrest, which is believed to contribute to aging and aging-related diseases. IPF is an age-related, chronic, progressive, and ultimately fatal interstitial lung disease of unknown etiology. IPF is characterized by repeated alveolar epithelial cell damage, fibroblast proliferation, excessive extracellular matrix (ECM) deposition, impaired gas exchange, and death. As an important transcription factor, p53 is critically involved in the regulation of senescence and fibrosis-related diseases. The mechanism of p53-mediated cellular senescence in IPF remains poorly understood, particularly regarding therapeutic strategies targeting p53. In this review, we summarize p53's structure, function, and signaling in senescence-driven IPF, and explore p53-targeted interventions for IPF. In conclusion, p53 may be a potential therapeutic target for senescence and IPF.