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• W2023157503 abstract "Autophagy is critical to the process of development because mouse models have shown that lack of autophagy leads to developmental arrest during the pre-implantation stage of embryogenesis. The process of autophagy is regulated through signaling pathways, which respond to the cellular environment. Therefore, any alteration in the environment may lead to the dysregulation of the autophagic process potentially resulting in cell death. Using both in vitro and in vivo models to study autophagy in the pre-implantation murine embryo, we observed that the cells respond to environmental stressors (i.e. hyperglycemic environment) by increasing activation of autophagy in a differential pattern within the embryo. This upregulation is accompanied by an increase in apoptosis, which appears to plateau at high concentrations of glucose. The activation of the autophagic pathway was further confirmed by an increase in GAPDH activity in both in vivo and in vitro hyperglycemic models, which has been linked to autophagy through the activation of the Atg12 gene. Furthermore, this increase in autophagy in response to a hyperglycemic environment was observed as early as the oocyte stage. In conclusion, in this study, we provided evidence for a differential response of elevated activation of autophagy in embryos and oocytes exposed to a hyperglycemic environment." @default.
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• W2023157503 date "2011-05-01" @default.
• W2023157503 modified "2023-10-03" @default.
• W2023157503 title "A differential autophagic response to hyperglycemia in the developing murine embryo" @default.
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• W2023157503 doi "https://doi.org/10.1530/rep-10-0265" @default.
• W2023157503 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/3831622" @default.
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