Does chronic blockade of class I PI3-kinase attenuate Ang II-induced cardiac hypertrophy and autophagic alteration?
These results demonstrate that class I PI3-kinase, via activation of the Akt-mTOR pathway, is involved in Ang II-induced impairment of autophagy, elevation of ROS, cardiac hypertrophy, and fibrosis, suggesting a novel target for cardiac protection.
These data indicate that physiologic concentrations of Fe3+ may act to modulate the depolarizing activity of circulating shock protein that in turn mediates the intracellular accumulation of salt and water in shock.