ABSTRACT
Idiopathic pulmonary fibrosis (IPF) is a progressive and fatal lung disease characterized by excessive collagen deposition and fibrosis of the lung parenchyma, leading to respiratory failure. The molecular mechanisms underlying IPF pathogenesis remain incompletely understood, hindering the development of effective therapeutic strategies. We have used a network medicine approach to comprehensively analyze molecular interactions and identify novel molecular signatures and potential therapeutics associated with IPF progression. Our integrative analysis revealed dysregulated molecular networks that are central to IPF pathophysiology. We have highlighted key molecular players and signaling pathways that are implicated in aberrant fibrotic processes. This systems-level understanding enables the identification of new biomarkers and therapeutic targets for IPF, providing potential avenues for precision medicine. Drug repurposing analysis revealed several drug candidates with anti-fibrotic, anti-inflammatory, and anti-cancer activities that could potentially slow fibrotic progression and improve patient outcomes. This study offers new insights into the molecular underpinnings of IPF and highlights network medicine approaches in uncovering complex disease mechanisms. The molecular signatures and therapeutic targets identified hold promise for developing precision therapies tailored to individual patients, ultimately advancing the management of this debilitating lung disease.