fig3

Role of MeCP2 in oligodendrocyte lineage cells in Rett syndrome: review and inference

Figure 3. Abnormal MeCP2 function may lead to changes in mitochondrial structure and function. MeCP2 may regulate the function of mitochondria by affecting electron transport chain complexes. The loss of MeCP2 function can lead to the release of cytochrome C into the cytoplasm and induce apoptosis. MeCP2 mutations can also lead to abnormal accumulation of reactive oxygen species, resulting in DNA damage and even apoptosis. However, an appropriate increase in ROS can make OPC exit the cell cycle and promote its differentiation. The abnormal function of MeCP2 can also reduce the coenzyme of dehydrogenase (NAD+) and the generation of ATP, thereby reducing the synthesis of lipids by affecting the reaction of tricarboxylic acid. OPC:oligodendrocyte precursor cell; ROS: reactive oxygen species.

Ageing and Neurodegenerative Diseases
ISSN 2769-5301 (Online)

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