Key result
Genistein inhibits isoproterenol-induced cardiac hypertrophy by increasing miR-451 and down-regulating TIMP2.
Why the study?
The underlying mechanisms of cardiomyocyte hypertrophy are not yet fully understood, motivating investigation of genistein's effects on isoproterenol-induced hypertrophy.
Does genistein reverse isoproterenol-induced cardiac hypertrophy in H9C2 cells and ICR mice?
Does genistein reverse isoproterenol-induced cardiac hypertrophy in H9C2 cells and ICR mice?
Genistein reverses isoproterenol-induced cardiac hypertrophy by regulating the miR-451/TIMP2 pathway in preclinical models.
Hypothesis-generating for genistein in hypertrophy; human translation remains unproven.
Cardiomyocyte hypertrophy, a prevalent clinical condition is deeply associated with many physiological factors. The underlying mechanisms of cardiomyocyte hypertrophy are not yet fully understood. In this study, H9C2 cells were treated with genistein, miR-451 mimic, miR-451 inhibitor and isoproterenol for 24 h, to study the effect of genistein on isoproterenol-induced myocardial hypertrophy in vitro. Simultaneously, ICR mice were treated with genistein for 21 days to evaluate the effects of the phytochemical on isoproterenol-induced myocardial hypertrophy in vivo. Results showed that isoproterenol induced cardiac hypertrophy and down-regulated the expression of miR-451 and up-regulated miR-451's target gene TIMP2. Genistein increased the expression of miR-451 and inhibited the isoproterenol-induced cardiac hypertrophy. This study explored the function of genistein from the epigenetic level, suggesting that miR-451 may play a significant role in the genistein-assisted amelioration of isoproterenol-induced cardiac hypertrophy both in vitro and in vivo.
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Gan et al. (2019) studied Isoproterenol-induced cardiac hypertrophy. Genistein vs. Isoproterenol alone was evaluated on Cardiac hypertrophy and expression of miR-451/TIMP2. Genistein inhibited isoproterenol-induced cardiac hypertrophy both in vitro and in vivo by increasing the expression of miR-451 and down-regulating its target gene TIMP2.
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