Table 1.

Selected microRNAs implicated in IPF

MicroRNAs	Observed Change	Physiological Consequence	Reference
miR-199a-5p	Upregulated in the bleomycin model and in samples from IPF patients	Key effector of TGF-β signaling in lung fibroblasts by regulating caveolin 1	62
miR-145	Increased in TGF-β1-treated lung fibroblasts and in the lungs of patients with IPF compared with normal human lungs	In lung fibroblasts, increased SMA-α expression, enhanced contractility, and promoted formation of focal and fibrillar adhesions; activation of latent TGF-β1	107
miR-155	Mouse model of lung fibrosis showed that miR-155 expression level was correlated with the degree of lung fibrosis	Participate in lung epithelial-mesenchymal interactions by binding to and decreasing the release of keratinocyte growth factor induced by IL-1β or TNF-α in human normal pulmonary fibroblasts	78
miR-200 family members	Reversing the fibrogenic activity of pulmonary fibroblasts from mice with experimental pulmonary fibrosis and from patients with IPF	Inhibited the TGF-β1-induced epithelial-mesenchymal transition of alveolar epithelial cells	106

Shown are selected microRNAs implicated in IPF; see text for others.