Constitutive activation of the PI3K-Akt-mTORC1 pathway sustains the m.3243 A > G mtDNA mutation

Constitutive activation of the PI3K-Akt-mTORC1 pathway sustains the m.3243 A > G mtDNA mutation

Heteroplasmic mtDNA mutations cause disease in humans. Here, Chung et al find the PI3K-Akt-mTORC1 pathway constitutively activated in cells with the heteroplasmic m.3243 A > G mutation, and inhibition of the pathway cell autonomously reduces mutant mtDNA load and rescues mitochondrial bioenergeti...

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Autores principales: Chih-Yao Chung, Kritarth Singh, Vassilios N. Kotiadis, Gabriel E. Valdebenito, Jee Hwan Ahn, Emilie Topley, Joycelyn Tan, William D. Andrews, Benoit Bilanges, Robert D. S. Pitceathly, Gyorgy Szabadkai, Mariia Yuneva, Michael R. Duchen
Formato: article
Lenguaje:EN
Publicado: Nature Portfolio 2021
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Science
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Acceso en línea:https://doaj.org/article/b9f6630675044451be3ddb118624adeb
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Sumario:Heteroplasmic mtDNA mutations cause disease in humans. Here, Chung et al find the PI3K-Akt-mTORC1 pathway constitutively activated in cells with the heteroplasmic m.3243 A > G mutation, and inhibition of the pathway cell autonomously reduces mutant mtDNA load and rescues mitochondrial bioenergetics.

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