MFN1 and cardiac hypertrophy: A very recent study has identified miR-153-3p as a trigger of abnormal mitochondrial fission and hypertrophic response, mainly through the inhibition of Mfn1 translation, and both in vivo and in vitro experiments confirmed that the ablation of miR-153-3p could dramatically avoid mitochondrial fission as well as cardiac hypertrophy (61).