Genistein reverses isoproterenol-induced cardiac hypertrophy by regulating miR-451/TIMP2.

@article{Gan2019GenisteinRI,
  title={Genistein reverses isoproterenol-induced cardiac hypertrophy by regulating miR-451/TIMP2.},
  author={Mailin Gan and Ting Zheng and Linyuan Shen and Ya Tan and Yuan Fan and Surong Shuai and Lin Bai and Xuewei Li and Jinyong Wang and Shunhua Zhang and Li Zhu},
  journal={Biomedicine \& pharmacotherapy = Biomedecine \& pharmacotherapie},
  year={2019},
  volume={112},
  pages={
          108618
        }
}
  • M. Gan, Ting Zheng, Li Zhu
  • Published 1 April 2019
  • Biology
  • Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie
The Expression of microRNA in Adult Rat Heart with Isoproterenol-Induced Cardiac Hypertrophy
TLDR
The first to discover that LncMIAT may act as an miR-144 sponge in isoproterenol-induced cardiac hypertrophy was discovered, and these results enriched the understanding of miRNA in regulating cardiachypertrophy and provided a reference for preventing and treating cardiac hyperTrophy.
Taurine attenuates isoproterenol-induced H9c2 cardiomyocytes hypertrophy by improving antioxidative ability and inhibiting calpain-1-mediated apoptosis
TLDR
It is believed that taurine prevents ISO-induced H9c2 cardiomyocyte hypertrophy by inhibiting oxidative stress, intracellular Ca 2+ overload, the calpain-1-mediated mitochondria-dependent apoptotic pathway and cleaved caspase-9 levels.
Genistein inhibits high fat diet-induced obesity through miR-222 by targeting BTG2 and adipor1.
TLDR
It is found that genistein can inhibit obesity and downregulate the expression of miR-222 in mouse adipose tissue and this findings provide a new epigenetic mechanism underpinning the ability ofgenistein to resist obesity.
MicroRNA-451 and Genistein Ameliorate Nonalcoholic Steatohepatitis in Mice
TLDR
This study shows that miR-451 has a protective effect on hepatic inflammation, and genistein can be used as a natural promoter of miR -451 to ameliorate NASH.
Genistein Alleviates High-Fat Diet-Induced Obesity by Inhibiting the Process of Gluconeogenesis in Mice
TLDR
It is found that genistein may inhibit gluconeogenesis in obese mice by regulating the expression of Gk and G6pc through miR-451, and the dual-luciferase reporter system showed that G 6pc (glucose-6-phosphatase) may be a target gene of miR -451.
Ellagic Acid Prevents Ca2+ Dysregulation and Improves Functional Abnormalities of Ventricular Myocytes via Attenuation of Oxidative Stress in Pathological Cardiac Hypertrophy.
TLDR
Protein expression analyses indicated that the upregulated p-PLB and p-CaMKII expressions were restored by EA treatment, suggesting improved calcium handling in the ISO + EA rat heart, whereas ISO rats displayed significantly increased expression of p-22phox and p47phox subunits of NOX2 protein.
Therapeutic potential of IKK-β inhibitors from natural phenolics for inflammation in cardiovascular diseases
TLDR
Icariin, salvianolic acid B, and plantainoside D are the most promising IKKβ inhibitors, and these phytochemicals could be helpful to find the lead compounds on designing and developing novel cardioprotective agents.
ssc-miR-451 Regulates Porcine Primary Adipocyte Differentiation by Targeting ACACA
TLDR
The effect of ssc-miR-451 on porcine adipose development and meat quality is reported and it is suggested that s sc-mi R-451 regulates lipid deposition and fatty acid composition by targeting ACACA, and sSc-mi-451 may serve as a potential genetic marker to improve pork quality.
Mechanism of the Regulatory Effect of Overexpression of circMTO1 on Proliferation and Apoptosis of Hepatoma Cells via miR-9-5p/NOX4 Axis
TLDR
Overexpression of CircMTO1 acts as tumor suppressor in liver cancer by sponging miR-9-5p, which upregulates NOX4, which increases the cell apoptosis rates.
miR-451 suppresses the malignant characteristics of colorectal cancer via targeting SAMD4B
TLDR
The miR-451/SAMD4B axis may serve as a novel therapeutic target in patients with CRC and is essential for blocking tumor growth via targeting S AMD4B in vivo and in vitro.
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Tanshinone IIA attenuated cardiomyocyte hypertrophy induced by ISO through inhibiting Calcineurin/NFATc3 pathway, which provides new insights into the pharmacological role and therapeutic mechanism of Tanshin one IIA in heart diseases.
E2/ER β inhibit ISO-induced cardiac cellular hypertrophy by suppressing Ca2+-calcineurin signaling
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Genistein attenuates pathological cardiac hypertrophy in vivo and in vitro
TLDR
Genistein attenuated pressure overload-induced cardiac hypertrophy in vivo and PE induced NRCM hypertropy in vitro and could not attenuate PE-induced cardiomyocyte hypertrophia even after pretreatment with sp61005 (a selective inhibitor of JNK1/2).
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Genistein prevents isoproterenol-induced cardiac hypertrophy in rats.
TLDR
The present study suggests that the salutary effects of genistein on isoproterenol-induced cardiac hypertrophy may be mediated through inhibition of iNOS and potentiation of eNOS activities.
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A novel insight is provided into the potential underlying mechanisms of telmisartan-induced inhibition of cardiomyocyte hypertrophy, which involves inhibition of NFAT activation, nuclear translocation and the ANP/BNP cascade.
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TLDR
In conclusion, this in vivo study showed that tanshinone IIA could improve heart function by enhancing myocardial contractility, inhibiting ECM deposition, and limiting apoptosis of cardiomyocytes and oxidative damage.
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TLDR
The findings indicate that miR‐451 regulates cardiac hypertrophy and cardiac autophagy by targeting TSC1, and may be a potential therapeutic target for this disease.
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TLDR
It is found that elevated miR-499 levels caused cellular hypertrophy and cardiac dysfunction in a dose-dependent manner and may titrate the cardiac response to stress in part by regulating the immediate early gene response.
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