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. Author manuscript; available in PMC: 2015 Apr 13.
Published in final edited form as: Cardiology. 2015 Mar 12;130(4):211–220. doi: 10.1159/000369782

Figure 6.

Figure 6

Proposed mechanism by which metabolic remodeling precedes and triggers structural and functional remodeling in the heart. Sustained pressure overload leads to increased glucose metabolism. However, a mismatch between glucose uptake and oxidation leads to accumulation of glucose 6-phosphate (G6P). This metabolite activates the mechanistic target of rapamycin complex 1 (mTORC1) by unknown mechanisms, resulting in increased protein synthesis and endoplasmic reticulum (ER) stress. As a consequence, the heart hypertrophies (increased protein synthesis) and fails (contractile dysfunction induced by ER Stress). Metformin and rapamycin decrease mTOR activity and may thus prevent LVH and HF. AMPK: 5′AMP-activated protein kinase. HK: Hexokinase-II. LVH: Left ventricular hypertrophy.