Akt3 is a target of miR-29c-3p and serves an important function in the pathogenesis of congenital heart disease.
Chen, Tao; Li, Shu-Jun; Chen, Bin; Huang, Qiong; Kong, Xiang-Ying; Shen, Chen; Gu, Hai-Tao; Wang, Xiao-Wei.
Int J Mol Med
; 43(2): 980-992, 2019 Feb.
Artigo em Inglês | MEDLINE | ID: mdl-30535467
Inhibition of miR-182-5p protects cardiomyocytes from hypoxia-induced apoptosis by targeting CIAPIN1.
miR-22 regulates starvation-induced autophagy and apoptosis in cardiomyocytes by targeting p38α.
Long noncoding RNA SNHG6 contributes to ventricular septal defect formation via negative regulation of miR-101 and activation of Wnt/ß-catenin pathway.
MiR-320 regulates cardiomyocyte apoptosis induced by ischemia-reperfusion injury by targeting AKIP1.
[Inhibition of microRNA195 attenuates high-glucose induced neonatal cardiomyocytes hypertrophy in vitro].
The miR-17-92 cluster regulates FOG-2 expression and inhibits proliferation of mouse embryonic cardiomyocytes.
Mir-190b negatively contributes to the Trypanosoma cruzi-infected cell survival by repressing PTEN protein expression.
miR-30c regulates proliferation, apoptosis and differentiation via the Shh signaling pathway in P19 cells.
Serum extracellular vesicles promote proliferation of H9C2 cardiomyocytes by increasing miR-17-3p.
miR-138 protects cardiomyocytes from hypoxia-induced apoptosis via MLK3/JNK/c-jun pathway.