Background: Cardiac fibrosis play a key role in the atrial fibrillation pathogenesis but the underlying potential\nmolecular mechanism is still understood. However, potential mechanisms for miR-21 upregulation and its role in\ncardiac fibrosis remain unclear. The controls cell proliferation and processes fundamental to disease progression.\nMethods: In this study, immunohistochemistry, real-time RT-PCR, cell transfection, cell cycle, cell proliferation and\nWestern blot were used, respectively.\nResults: Here we have been demonstrated that the tumor suppressor cell adhesion molecule 1 (CADM1) is the\npotential target of miR-21. Our study revealed that miR-21 regulation of CADM1 expression, which was decreased\nin cardiac fibroblasts and fibrosis tissue. The cardiac fibroblasts transfected with miR-21 mimic promoted miR-21\noverexpression enhanced STAT3 expression and decreased CADM1 expression. Nevertheless, the cardiac fibroblasts\ntransfected with miR-21 inhibitor obtained the opposite expression result. Furthermore, downexpression of miR-21\nsuppressed cardiac fibroblast proliferation.\nConclusions: These results suggested that miR-21 overexpression promotes cardiac fibrosis via STAT3 signaling\npathway by decrease CADM1 expression, indicating miR-21 as an important signaling molecule for cardiac fibrotic\nremodeling and AF.
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