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Idiopathic pulmonary fibrosis (IPF) remains a fatal, heterogeneous disease in which clinicians lack reliable tools to anticipate trajectory or tailor therapy.1 While there are two approved antifibrotic medications for IPF worldwide and a third recently approved in the US and China, their effects are modest, underscoring the need for minimally invasive biomarkers that reflect disease activity in the lung and define biologically relevant endotypes to guide personalised treatment.2–4 In this issue of Thorax, Yang and colleagues evaluate CTHRC1—an emerging molecular target in the field of fibrotic lung disease—as a prognostic biomarker in IPF.5