Title : EGCG Blocked Phenylephrin-Induced Hypertrophy in H9C2 Cardiomyocytes, by Activating AMPK-Dependent Pathway.

Pub. Date : 2015 May

PMID : 25954124






6 Functional Relationships(s)
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1 EGCG Blocked Phenylephrin-Induced Hypertrophy in H9C2 Cardiomyocytes, by Activating AMPK-Dependent Pathway. epigallocatechin gallate protein kinase AMP-activated catalytic subunit alpha 2 Homo sapiens
2 Moreover, we showed that AMPK is activated in H9C2 cardiomyocytes by EGCG, and AMPK-dependent pathway participates in the inhibitory effects of EGCG on cardiac hypertrophy. epigallocatechin gallate protein kinase AMP-activated catalytic subunit alpha 2 Homo sapiens
3 Moreover, we showed that AMPK is activated in H9C2 cardiomyocytes by EGCG, and AMPK-dependent pathway participates in the inhibitory effects of EGCG on cardiac hypertrophy. epigallocatechin gallate protein kinase AMP-activated catalytic subunit alpha 2 Homo sapiens
4 Moreover, we showed that AMPK is activated in H9C2 cardiomyocytes by EGCG, and AMPK-dependent pathway participates in the inhibitory effects of EGCG on cardiac hypertrophy. epigallocatechin gallate protein kinase AMP-activated catalytic subunit alpha 2 Homo sapiens
5 Taken together, our findings provide the first evidence that the effect of EGCG against cardiac hypertrophy may be attributed to its activation on AMPK-dependent signaling pathway, suggesting the therapeutic potential of EGCG on the prevention of cardiac remodeling in patients with pressure overload hypertrophy. epigallocatechin gallate protein kinase AMP-activated catalytic subunit alpha 2 Homo sapiens
6 Taken together, our findings provide the first evidence that the effect of EGCG against cardiac hypertrophy may be attributed to its activation on AMPK-dependent signaling pathway, suggesting the therapeutic potential of EGCG on the prevention of cardiac remodeling in patients with pressure overload hypertrophy. epigallocatechin gallate protein kinase AMP-activated catalytic subunit alpha 2 Homo sapiens