Figure 8
A proposed model that depicts the potential mechanisms by which high glucose exposure leads to defects in cranial neural crest cell generation.
High levels of glucose might trigger autophagic disturbances and promote ERK activation. The expression of the neural crest development-related genes Pax3, Sox9 and Slug were also adversely influenced. It is well known that elevated levels of glucose can also induce autophagy through ER stress, although we did not address this mechanism in the current study. In summary, we propose that excessive cell autophagy induced by high glucose levels is the key factor that induces increased apoptosis in the cranial neural crest.
