MicroRNA-323a-3p Promotes Pressure Overload-Induced Cardiac Fibrosis by Targeting TIMP3

Conclusion: Our findings provide evidence that miR-323a-3p promotes cardiac fibrosis via miR-323a-3p-TIMP3-TGF- β pathway. miR-323a-3p may be a new marker for cardiac fibrosis progression and that inhibition of miR-323a-3p may be a promising therapeutic target for the treatment of cardiac fibrosis.Cell Physiol Biochem 2018;50:2176 –2187

https://www.karger.com/Article/FullText/495059

Source: Cellular Physiology and Biochemistry - November 9, 2018 Category: Cytology Source Type: research