https://www.selleckchem.com/products/arry-382.html
01). miR-101 overexpression inhibited the increasing of autophagy and apoptosis in mice and in myocardial cells (p less then 0.01). DDIT4 was a target gene of miR-101 and expressed increasingly in MI-induced injury mice and hypoxia treated myocardial cells. miR-101 could negatively regulated the expression of DDIT4. CONCLUSION This research suggested that miR-101 attenuatedMI-induced injury by targeting DDIT4 to regulate autophagy, which indicated that miR-101 or DDIT4 may be potential therapeutic targets for heart injury. Copyright© B
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