MiR-326 targets MDK to regulate the progression of cardiac hypertrophy through blocking JAK/STAT and MAPK signaling pathways.

Cardiac hypertrophy is a heart reaction to the increase of cardiac load, with the characteristics of increased expression of cardiac hypertrophy markers, enhanced protein synthesis, and enlarged cell area. However, molecular mechanisms in cardiac hypertrophy are still poorly substantiated. It has been reported that miRNAs can modulate human diseases, among which miR-326 has been reported as a biological regulator in human cancers, but its role in cardiac hypertrophy is rarely explored. This study focused on the exploration of the potential of miR-326 in cardiac hypertrophy. Our data revealed the downregulation of miR-326 in the TAC-induced hypertrophic mice and the Ang II-induced hypertrophic H9c2 cells. Functionally, miR-326 attenuated the effect of Ang II on cardiac hypertrophy in vitro. In addition, miR-326 negatively regulated and MAPK signaling pathways. Mechanistically, miR-326 targeted and inhibited MDK to induce JAK/duanyu1813 and MAPK pathways. Rescue assays certified that miR-326 attenuated cardiac hypertrophy through targeting MDK and inhibiting JAK/duanyu1813 and MAPK signaling pathways. In brief, our study unveiled that miR-326 targets MDK to regulate the progression of cardiac hypertrophy through blocking JAK/duanyu1813 and MAPK signaling pathways, indicating that targeting miR-326 as a potential approach for cardiac hypertrophy treatment.

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