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Fig. 6 | Diabetology & Metabolic Syndrome

Fig. 6

From: Maternal hyperglycemia inhibits pulmonary vasculogenesis during mouse fetal lung development by promoting GβL Ubiquitination-dependent mammalian target of Rapamycin assembly

Fig. 6

The proposed mechanism of hyperglycemia inhibits pulmonary vasculogenesis. Maternal hyperglycemia can up-regulate the expression level of TRAF2 in mouse fetal lung, which acts as an E3 ligase in the regulation of mTORC1 and mTORC2 formation. By promoting the polyubiquitination of GβL, up-regulated TRAF2interferes with the interaction of GβL with SIN1 (a unique component of mTORC2), which promotes the formation of mTORC1, thus inhibiting mouse fetal lung angiogenesis.↑represents the up-regulated expression levels of TRAF2, GβL-ubiquitination, and mTORC1 assembly;↓represents down-regulation of mTORC2 assembly; indicates promotion of the events; indicates inhibition of the events.

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