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Idiopathic pulmonary fibrosis (IPF) is a chronic, progressive interstitial lung disease characterized by deregulated cell death programs that drive epithelial injury, fibroblast activation, and irreversible tissue remodeling. Multiple regulated cell death (RCD) modalities, including apoptosis, autophagy, necrosis, ferroptosis, pyroptosis, and cuproptosis, are implicated in IPF pathogenesis across epithelial cells, fibroblasts, macrophages, and endothelial cells. Apoptosis leads to alveolar epithelial cell loss and fibrosis initiation, whereas autophagy modulates fibroblast proliferation and extracellular matrix turnover. Necrosis amplifies inflammation; ferroptosis promotes epithelial dysfunction through lipid peroxidation; and pyroptosis activates the inflammasome pathway. Emerging evidence links cuproptosis, a copper-dependent death mode, to fibrotic remodeling. These pathways are interconnected: apoptosis and autophagy can shift within the same cell, and epithelial apoptosis may induce macrophage pyroptosis, amplifying the profibrotic cascade. Emerging evidence indicates that these RCD modalities are coordinated through shared stress signals and regulatory nodes. Therapeutically, targeting RCD offers promising opportunities, with Bcl-2 inhibitors for apoptosis, mTOR inhibitors for autophagy, iron chelators for ferroptosis, and early interventions for pyroptosis and cuproptosis. Targeting shared regulatory mechanisms or combining pathway-directed strategies may further enhance efficacy. By balancing cell death and survival, these strategies could attenuate inflammation, restrict fibroblast-driven scarring, and restore repair capacity. This review underscores the complexity and crosstalk of RCD in IPF, and proposes a conceptual framework for their coordinated regulation, highlighting its potential for therapeutic innovation.