<p>Pulmonary fibrosis (PF) is a pathological change in the development of end-stage lung disease, referring to an irreversible lesion in which lung tissue undergoes an abnormal repair response during injury repair, resulting in the replacement of normal alveolar structure by fibrous scarring. The main mechanisms of pulmonary fibrosis progression are activation of epithelial cell and macrophage repair after oxidative stress, fibroblast proliferation leading to extracellular matrix deposition in the lung, and a repair process involving multiple modes of death and molecular mechanisms that cross-talk in macrophages and alveolar epithelial cells, accelerating extracellular matrix deposition. Cell death is controlled by programmed cell death (PCD), which mainly includes apoptosis, necrotic apoptosis, pyroptosis, ferroptosis and autophagy. There is increasing evidence that PCD plays an important role in the pathogenesis of pulmonary fibrosis progression. In this review, we discuss recent advances in the role of PCD in lung injury-accelerated fibrosis, show how the mode of death of alveolar epithelial cells, macrophages, and fibroblasts promotes or inhibits the progression of lung injury, and explore associations between different types of PCD, with the aim of exploring the molecular mechanisms underlying the progression of recurrent lung injury and searching for new therapeutic targets.</p>