Key result
In TNF-α-induced hypertrophic cardiomyocytes, exercise-mimicking AICAR treatment inhibited Traf2 up-regulation and Akt acetylation, while resveratrol promoted FOXO1 deacetylation.
In an in vitro model of cardiac hypertrophy, the exercise mimetic AICAR inhibited TNF-α-induced Traf2 up-regulation and Akt acetylation, suggesting a mechanism for the benefits of exercise in cardiac hypertrophy.
Changes of Traf2 and SIRT1 Expression by AICAR
No takes yet. Share an insight, caveat, or question.
Kim et al. (2017) studied Cardiac hypertrophy (in vitro model). AICAR and SIRT1 activator (resveratrol) vs. Control cells or TNF-α alone was evaluated on Traf2 and SIRT1 expression, Akt and FOXO1 phosphorylation/acetylation. In TNF-α-induced hypertrophic cardiomyocytes, exercise-mimicking AICAR treatment inhibited Traf2 up-regulation and Akt acetylation, while resveratrol promoted FOXO1 deacetylation.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: