About half of people diagnosed with idiopathic pulmonary fibrosis (IPF), in which patches of lung become damaged, die within three to five years of diagnosis. To probe the mechanisms behind this disease, a Yale-led collaboration investigated the gene expression patterns found in samples from fibrotic and healthy human lungs.
Naftali Kaminski, MD, Boehringer Ingelheim Pharmaceuticals, Inc. Endowed Professor of Medicine (Pulmonary), and colleagues took multiple samples to capture different levels of fibrosis. Their results were published in JCI Insight.
Levels of fibrosis-associated gene products did not gradually increase or decrease as samples became more fibrotic. Rather, different RNA molecules—messenger RNAs and microRNAs—characterized distinct stages of the disease. Further gene-expression changes seemed to recede fibrosis. In lungs from IPF patients, non-fibrotic samples that appeared similar to those from control lungs nonetheless had very different patterns of gene expression.
Knowledge of gene expression changes associated with each stage of disease should help researchers develop stage-specific therapies, the authors write.