Then, miR-200c was predicted and convinced to be a direct target of MALAT1, and high-mobility group box 1 (HMGB1) was verified to be a target of miR-200c during arrhythmia.
Our study establishes the role of f-channels in cardiac automaticity and indicates that arrhythmia related to HCN loss-of-function may be managed by pharmacological or genetic inhibition of GIRK4 channels, thus offering a new therapeutic strategy for the treatment of heart rhythm diseases.