:Idiopathic pulmonary fibrosis (IPF) is an interstitial lung disease characterized by progressive scarring of the lung tissue, with a poor prognosis and a median survival of only 3–5 years.The precise molecular mechanisms underlying IPF remain incompletely elucidated, and effective targeted drugs are lacking. Therefore, defining its pathogenesis is crucial. Ferroptosis, a regulated form of cell death driven by iron-dependent lipid peroxidation, has been identified as a key player in IPF. Emerging studies into ferroptosis have revealed the roles of cell-cell interactions in IPF disease mechanisms at the cellular level. This article provides a summarized overview of the mechanism by which cellular interactions contribute to iron-dependent pulmonary fibrosis through ferroptosis.