Idiopathic pulmonary fibrosis (IPF) is a chronic lung disease characterized by alveolar epithelial cell injury, aberrant repair, and pathological fibrosis. Recent studies have identified ferroptosis, as an irondependent, lipid peroxidation-driven form of programmed cell death, as a critical factor in the pathogenesis of IPF.This review elaborates on the fundamental pathological contributions of type Ⅱ alveolar epithelial cells, fibroblasts/ myofibroblasts, and macrophages in IPF, and analyzes the hallmarks of ferroptosis and its association with the characteristic pathological alterations of IPF, namely oxidative stress and dysregulated iron metabolism. Finally, we consider the cellular crosstalk mechanisms from the perspectives of the vicious cycle of paracrine signaling, receptorligand-mediated iron metabolic reprogramming, extracellular matrix-integrin-mediated mechanical stress, and cellular phenotypic reprogramming. A deeper understanding of this intricate cellular interaction network, particularly the pivotal regulatory role of ferroptosis, will provide a crucial theoretical foundation for the development of novel multitarget combination therapeutic strategies.