Idiopathic pulmonary fibrosis (IPF) is a progressive pulmonary disease of unknown origin with a high mortality rate and limited treatment options. Fibroblasts are central to matrix homoestasis and thus critical for the development and progression of IPF. Cellular senescence plays an important, however, controversially discussed role in IPF for having both pro- and anti-fibrotic effects. Senescent lung fibroblasts have been reported to express increased amounts of miRNA34a, which has anti-fibrotic effects and promotes apoptosis in the cells that express it. However, nothing is known about the levels of miRNA34a in exosomes as providers of intercellular communication.