Idiopathic pulmonary fibrosis (IPF) is a chronic interstitial lung disease with limited treatment options and a poor prognosis. Lung cancer (LC) is one of the most common comorbidities in IPF, and IPF is recognized as an independent risk factor for the development of LC. In recent years, increasing evidence has suggested that these two diseases may share convergent genetic, epigenetic and cellular mechanisms, particularly within their microenvironments.

A comprehensive literature search was performed across PubMed, Web of Science, and Google Scholar databases to identify relevant studies focusing on the shared cellular components, immune and stromal behaviors, and pathogenic pathways within the microenvironments of IPF and LC.

This review delineates the convergent features of the IPF and LC microenvironments by synthesizing the functional reprogramming of key cellular constituents. The immunological landscape is characterized by aberrant macrophage polarization, T-cell exhaustion and the accumulation of immunosuppressive myeloid-derived suppressor cells and immature dendritic cells. Furthermore, profound stromal alterations are observed, encompassing fibroblast activation, pathological extracellular matrix remodelling, epithelial–mesenchymal transition and dysregulated angiogenesis. These common cellular and molecular alterations may simultaneously drive fibrosis progression and tumorigenesis.

A deeper understanding of the relationship between the IPF and LC microenvironments will help identify shared pathological mechanisms and provide new insights for developing more targeted diagnostic and therapeutic strategies for idiopathic pulmonary fibrosis associated with lung cancer (IPF-LC).