Myofibroblasts as key effector cells in fibrotic lesions, exhibit apoptosis resistance as a core factor contributing to the persistent progression and refractory reversal of fibrosis. This article systematically investigates their role in pulmonary fibrosis by focusing on the origin and regulation of myofibroblasts, the mechanisms underlying apoptosis resistance, and the association between cellular senescence and apoptosis resistance. Key analyses include the molecular regulatory network of apoptosis resistance, metabolic and epigenetic mechanisms, immune evasion pathways, and the regulatory effects of cellular senescence on apoptosis processes. These findings aim to provide novel insights for elucidating the pathogenesis of pulmonary fibrosis and guiding therapeutic drug development.