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Integrated 'Omics in Idiopathic Pulmonary Fibrosis: Where Do We Go from Here?
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Integrated 'Omics in Idiopathic Pulmonary Fibrosis: Where Do We Go from Here?
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Integrated 'Omics in Idiopathic Pulmonary Fibrosis: Where Do We Go from Here?
Integrated 'Omics in Idiopathic Pulmonary Fibrosis: Where Do We Go from Here?
Journal Article

Integrated 'Omics in Idiopathic Pulmonary Fibrosis: Where Do We Go from Here?

2021
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Overview
Innovative studies with 'omics technologies have led to important insights into the pathophysiology of idiopathic pulmonary fibrosis (IPF). Studies using single-cell transcriptomics have demonstrated the role of novel epithelial and immune cell types in IPF lungs by identifying novel profibrotic alveolar macrophage populations and dedifferentiated epithelial cell populations that secrete profibrotic mediators. Genetic studies of familial pulmonary fibrosis have identified disease-causing genetic variants that disrupt genes involved in telomere maintenance, surfactant production, and mitochondrial functions, and studies of sporadic IPF have identified 14 genome-wide significant associations, including the particularly strong association with a promoter variant causing increased expression of MUC5B. As in many other 'omics studies of IPF lung tissue, the sheer volume of associations can be overwhelming, and it is a challenge to make sense of the thousands of differentially associated RNAs, miRNAs, proteins, and methylated DNA regions.