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. 2018 Aug 17;9:903. doi: 10.3389/fphar.2018.00903

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Copyright © 2018 Li, Zhou and Tang.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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The proposed mechanisms for the reciprocal repression between calcineurin and miR-133 in hypertrophic heart. (A) Either exogenous miR-133 supplement or endogenous miR-133 increase gives rise to the transcriptional repression of calcineurin and suppression of NFAT, causing the increased miR-133 level. Eventually, the increased miR-133 further enhanced miR-133 expression. (B) The calcineurin/ NFAT signaling is activated by pathological stimuli, giving rise to the downregulation of miR-133 expression. The decreased miR-133 induces the enhancement of calcineurin transcription. Consequently, the activated calcineurin triggers the further increase of calcineurin/ NFAT pathway. ↑, increase; ↓, decrease.