Targeting the AXL pathway: a promising strategy for pulmonary fibrosis

Idiopathic pulmonary fibrosis (IPF) is a chronic, progressive interstitial lung disease characterised by the accumulation of aberrant fibrotic tissue that is irreversible and results in impaired pulmonary function and respiratory failure. Globally, IPF affects approximately 3 million individuals, with an annual incidence rate of 3–9 cases per 100 000 people in North America and Europe [1]. Median survival following diagnosis is estimated to be between 3 and 5 years, with a 5-year survival rate comparable to that of many aggressive malignancies [2]. Significant advancements in the management of IPF have been made with the development of antifibrotic therapies that slow disease progression. Of the approved therapies, nintedanib is a tyrosine kinase inhibitor that targets multiple receptors, including vascular endothelial growth factor, fibroblast growth factors and platelet-derived growth factor [3]. Given the central role of receptor tyrosine kinases (RTKs) within IPF, there is growing interest in their potential to understand the mechanisms underlying disease progression and inform targeted therapeutic strategies.