Imre Noth,¹ Janine Roy,² Ramona Schmid,³ Richard Vinisko,⁴ Benjamin Strobel,³ Megan L Neely,^5,6 Christian Hesslinger,³ John A Belperio,⁷ Kevin R Flaherty,⁸ Margaret L Salisbury,⁹ Justin Oldham,¹⁰ Scott M Palmer,^5,6 Jamie L Todd,^5,6 Thomas B Leonard⁴ on behalf of the IPF-PRO™ Registry investigators

¹Division of Pulmonary and Critical Care Medicine, University of Virginia, Charlottesville, Virginia, USA; ²Staburo GmbH, Munich, Germany; ³Boehringer Ingelheim Pharma GmbH & Co. KG, Biberach, Germany; ⁴Boehringer Ingelheim Pharmaceuticals Inc., Ridgefield, Connecticut, USA; ⁵Duke Clinical Research Institute, Durham, North Carolina, USA; ⁶Duke University Medical Center, Durham, North Carolina, USA; ⁷David Geffen School of Medicine at UCLA, Los Angeles, California, USA; ⁸Division of Pulmonary and Critical Care Medicine, University of Michigan, Ann Arbor, Michigan, USA; ⁹Vanderbilt University, Nashville, Tennessee, USA; ¹⁰Department of Internal Medicine, Division of Pulmonary and Critical Care Medicine, University of California at Davis, Sacramento, California, USA.

Introduction

Idiopathic pulmonary fibrosis (IPF) is a progressive fibrosing interstitial lung disease characterized by decline in lung function.
MicroRNAs are small non-coding RNA molecules with functions in gene silencing or post-transcriptional gene regulation. Altered microRNA expression has been implicated in the pathogenesis of IPF.¹
Further investigation is needed to understand the relationships between messenger RNAs (mRNAs) and microRNAs and progression of IPF.