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Comment
. 2009 Jul;17(1):6-8.
doi: 10.1016/j.devcel.2009.07.004.

TGF-beta: a new role for an old AktTOR

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Comment

TGF-beta: a new role for an old AktTOR

Pankuri Goraksha-Hicks et al. Dev Cell. 2009 Jul.

Abstract

Nutrient overabundance is known to promote cellular hypertrophy, a significant pathological event in diseases like diabetes and cancer, although mechanisms have remained unclear. In this issue of Developmental Cell, Wu and Derynck provide a new model that links metabolism and cell growth by demonstrating that hyperglycemia can increase TGF-beta-dependent activation of the mTOR pathway to promote cellular hyperplasia.

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Figure 1
Figure 1. Model of Glucose-Stimulated Cellular Hypertrophy
Hyperglycemia increases TGF-β signaling through two proposed mechanisms (red dashed arrows). Glucose overabundance led to increased cell surface levels of TβRI and RII as well as activation and processing of latent TGF-β by MMP-2 and MMP-9. Cellular hypertrophy is caused by Smad-independent activation of the PI3K/Akt/mTOR pathway.

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