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. 2015 Sep;6(5):519-21.
doi: 10.1111/jdi.12317. Epub 2015 Jan 8.

Epidermal growth factor receptor signaling and the progression of diabetic nephropathy

Daisuke Koya  1
Affiliations

Epidermal growth factor receptor signaling and the progression of diabetic nephropathy

Daisuke Koya. J Diabetes Investig. 2015 Sep.
No abstract available

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Figures

Figure 1
Figure 1
Diabetes mellitus-related endoplasmic reticulum (ER) stress is a potent pathogenic factor of diabetic nephropathy. Healthy kidney cells have the ability to induce autophagy to overcome prolonged ER stress conditions, leading to kidney protection (blue lines and boxes). Autophagy is negatively and positively regulated by two intracellular nutrient signals, mammalian target of rapamycin complex 1 (mTORC1) and adenosine monophosphate-activated protein kinase (AMPK), respectively. Diabetes mellitus-related hypernutrient condition activates mTORC1 and suppresses AMPK, leading to autophagy inhibition through the inactivation of UNC-51-like kinase 1 (ULK1), a critical regulatory protein to initiate autophagy. Altered intracellular nutrient-sensing signal-mediated autophagy inhibition is involved in the progression of diabetic nephropathy via the enhancement of ER stress (red lines and boxes). Epidermal growth factor receptor (EGFR) inhibition slows the progression of diabetic nephropathy with a reduction in ER stress and an increase in autophagy by amelioration of altered nutrient-sensing signals (light blue line and box).
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