AMPKα2 counteracts the development of cardiac hypertrophy induced by isoproterenol

E Zarrinpashneh, C Beauloye, A Ginion… - Biochemical and …, 2008 - Elsevier
E Zarrinpashneh, C Beauloye, A Ginion, AC Pouleur, X Havaux, L Hue, B Viollet…
Biochemical and biophysical research communications, 2008Elsevier
As AMP-activated protein kinase (AMPK) controls protein translation, an anti-hypertrophic
effect of AMPK has been suggested. However, there is no genetic evidence to confirm this
hypothesis. We investigated the contribution of AMPKα2 in the control of cardiac hypertrophy
by using AMPKα2−/− mice submitted to isoproterenol. The isoproterenol-induced cardiac
hypertrophy, measured by left ventricular mass and histological examination, was
significantly higher in AMPKα2−/− than in WT animals. Moreover, the intensification of …
As AMP-activated protein kinase (AMPK) controls protein translation, an anti-hypertrophic effect of AMPK has been suggested. However, there is no genetic evidence to confirm this hypothesis. We investigated the contribution of AMPKα2 in the control of cardiac hypertrophy by using AMPKα2−/− mice submitted to isoproterenol. The isoproterenol-induced cardiac hypertrophy, measured by left ventricular mass and histological examination, was significantly higher in AMPKα2−/− than in WT animals. Moreover, the intensification of cardiac hypertrophy found in AMPKα2−/− mice can be linked to the abnormal basal overstimulation of the p70 ribosomal S6 protein kinase, an enzyme known to regulate protein translation and cell growth. In conclusion, this work shows that AMPKα2 plays a role of brake pedal for the development of cardiac hypertrophy.
Elsevier