Studies utilizing RNA sequencing and single-cell approaches have identified new cell types, genes, and pathways that contribute to the pathogenesis of lung fibrosis. However, layers of biologic data beyond the transcriptome, including genomic, epigenomic, proteomic, and metabolomic studies have also enhanced our understanding of fibrotic mechanisms. Understanding these multi-omic “universes” and how they interact with the environment and microbiome can help address fundamental questions regarding etiology, prognosis, and strategies for personalized treatment. This session will highlight the current state of knowledge in these other areas and attempt to integrate these data into a cohesive understanding of IPF pathogenesis.
• Understand and recognize how different biologic processes, including genomic, epigenomic, metabolomic, and microbiome changes contribute to the development and pathogenesis of IPF/ILD
• Learn how some of these diverse layers of biologic data can be integrated to derive new insights into IPF pathogenesis
• Identify challenges to integrating -omics data and identify areas for future research need in IPF/ILD
Ivana Yang, BS, PhD
Giovanni Ligresti, PhD
Oliver Eickelberg, MD, ATSF
Louise Hecker, PhD
David O'Dwyer, BM BCH, BMedSci, PhD
Naftali Kaminski, MD, ATSF
Into the Genomics and Epigenomics Universe of IPF
“ATAC”-ing IPF: how Understanding Chromatin Biology Sheds Light on Fibrosis
The next frontier: Proteomics of posttranslational modifications in IPF - Presentation withheld at the speaker's request
How Pharmacogenomics and Drug Discovery can Provide New Insights into ILD Pathogenesis
Understanding the systemic microbiome in IPF
The Multi-Omic Universe: How Do We Integrate These Datasets to Better Understand and Eventually Cure IPF