“…Although fibrotic interstitial lung disease limits the lesion site in the lung, it results in a series of pathological events, among which fibroblast proliferation and differentiation, apoptosis, autophagy, and inflammatory damage may ultimately lead to lung function failure [ 109 ]. Due perhaps to the chronic and progressive nature and severity of lung injury induced by pulmonary fibrosis, several profibrotic miRNAs are downregulated in lung tissue in response to pulmonary fibrosis, as previously shown for miR-21, miR-506, miR-96, miR-499a, miR-326, miR-410, miR-124, miR-328, miR-420, miR-7, miR-19a, miR-19b, miR-26b, miR-9, miR-29, and miR-30a [ 110 , 111 ]. In contrast, other antifibrotic miRNAs, such as miR-30, miR-101, miR-344, miR-323a-3p, miR-29b, miR-185, miR-29a, miR-185, miR-186, miR-221, miR-1343, miR-27a-3p, and miR-27b, are increased [ 110 , 111 ].…”