title: Towards systems biology of human pulmonary fibrosis.
abstract: The integrated effect of multiple pathways, molecules, genetic polymorphisms, environmental stimuli, and possible infection determines the lung phenotype in idiopathic pulmonary fibrosis (IPF), a chronic progressive and often lethal lung disease. Systems biology approaches aim to provide a systemwide view of biological process using computational tools and high-throughput technologies. Although much of the analysis of genome-level transcriptional high-resolution profiles of IPF was reductionist, usually focusing on a single factor in the disease process, there are some studies that implement systems approaches. We discuss these analyses and provide examples of the global analysis of IPF, hypersensitivity pneumonitis, and nonspecific interstitial pneumonia. Detailed quantitative phenotyping and correlation with microarray results as well as high-throughput genotyping should provide us with the datasets to implement systems biology approaches in fibrosis research. Interdisciplinary teams and training of junior investigators in the vocabulary of systems biology should allow us to use these datasets integratively and generate a global model of human pulmonary fibrosis.
authors.affiliation: Dorothy P. and Richard P. Simmons Center for Interstitial Lung Disease, Pulmonary, Allergy, and Critical Care Medicine, University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania, USA.
authors.forename: Sean M
authors.initials: SM
authors.lastname: Studer
authors.forename: Naftali
authors.initials: N
authors.lastname: Kaminski
mesh_terms: D000818:Animals; D004195:Disease Models, Animal; D016678:Genome; D006239:Haplotypes; D006801:Humans; D051379:Mice; D020411:Oligonucleotide Array Sequence Analysis; D010641:Phenotype; D011658:Pulmonary Fibrosis / Q000235:genetics* / Q000503:physiopathology; D051381:Rats; D049490:Systems Biology