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Dysregulated glycolysis has been noted in several pathological processes characterized by supporting cell proliferation. Nonetheless, the role of glycolysis reprogramming is not well appreciated in cardiac fibrosis which is accompanied by increased fibroblasts proliferation. In this study, we investigated the cause and consequence of glycolysis reprogramming in cardiac fibrosis, using clinical samples, animal models, and cultured cells. Herein, we report that methyltransferase-like 3 (METTL3) facilitates glycolysis and cardiac fibroblasts proliferation, leading to cardiac fibrosis. The augmentation of glycolysis, an essential event during cardiac fibroblasts proliferation, is dependent on an increased expression of METTL3. A knockdown of METTL3 suppressed glycolysis, and inhibited cardiac fibroblast proliferation and cardiac fibrosis. Mechanistically, METTL3 epigenetically repressed androgen receptor (AR) expression in an m |
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