Building translational bridges in idiopathic pulmonary fibrosis research: from epithelial dysfunction to dysregulated macrophage polarisation and fibrogenesis

Idiopathic pulmonary fibrosis (IPF) remains among the most devastating interstitial lung diseases (ILDs), marked by progression, impaired quality of life, poor prognosis and limited therapeutic options. Despite two approved antifibrotic compounds, nintedanib and pirfenidone, and probably a third to come (nerandomilast), IPF patients continue to face unfavourable outcomes, with no available therapy capable of halting or reversing fibrosis [1]. Scientific advancements have deepened our knowledge of many of the underlying pathophysiological mechanisms of IPF in recent years, unveiling molecular intricacies across epithelial, mesenchymal, endothelial and immune compartments. A series of articles published in this issue of the European Respiratory Journal have highlighted many of the key studies discussed here, underscoring the pace of discovery in IPF research. Yet, the translational bridges between discovery and clinical care remain fragile. The field now stands at a key point: whether we can translate scientific insights into real-world clinical implementation (figure 1).