Idiopathic pulmonary fibrosis (IPF) is a serious lung disease that involved the myofibroblast differentiation of lung resident mesenchymal stem cells (LR-MSCs). However, the specific molecular mechanisms of myofibroblast differentiation of LR-MSCs still remain a mystery. In this study, a comprehensive analysis of miRNAs and mRNAs changes in LR-MSCs treated with TGF-β1 was performed. Through computational approaches, the pivotal roles of differentially expressed miRNAs that were associated with tight junction, pathways in cancer, focal adhesion, and cytokine-cytokine receptor interaction were shown. Kruppel-like factor 4 (Klf4) and inhibitor of growth family, member 5 (Ing5) may be the targets for the therapy of pulmonary fibrosis by inhibiting myofibroblast differentiation of LR-MSCs and EMT. Collectively, a molecular paradigm for understanding myofibroblast differentiation of LR-MSCs in IPF was provided by the integrated miRNA/mRNA analyses.

特发性肺纤维化（IPF）是一种严重的肺部疾病，涉及肺驻留间充质干细胞（LR-MSC）的成纤维细胞分化。然而，LR-MSCs成纤维细胞分化的具体分子机制仍然是一个谜。在这项研究中，对TGF-β1处理的LR-MSC中miRNA和mRNA的变化进行了全面分析。通过计算方法，显示了与紧密连接，癌症途径，粘着斑和细胞因子-细胞因子受体相互作用相关的差异表达miRNA的关键作用。通过抑制LR-MSC和EMT的成纤维细胞分化，Kruppel样因子4（Klf4）和生长家族抑制剂成员5（Ing5）可能是治疗肺纤维化的靶标。总的来说，