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. 2018 Oct 23;68(1):141–155. doi: 10.2337/db18-0232

Figure 7.

Figure 7

Model for regulation of BMSCs by the Nrf2/Keap1 pathway and disruption in diabetes. In steady state, activation of the Nrf2/Keap1 pathway preserves redox metabolism, multipotency, and associated features of BMSCs. Nrf2 drives transcription of antioxidants, metabolic modulators, and Sox2 to maintain low ROS in BMSCs and maintain multipotency. In diabetes, loss of Nrf2-driven transcription, and therefore high intracellular ROS, promotes expression of adipogenic genes and leads to commitment of BMSCs to an adipogenic fate.