Human neural stem cell-derived artificial organelles to improve oxidative phosphorylation

Jiayi Wang, Mengke Zhao, Meina Wang, Dong Fu, Lin Kang, Yu Xu, Liming Shen, Shilin Jin, Liang Wang () and Jing Liu ()
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Jiayi Wang: The First Affiliated Hospital of Dalian Medical University
Mengke Zhao: The First Affiliated Hospital of Dalian Medical University
Meina Wang: The First Affiliated Hospital of Dalian Medical University
Dong Fu: The First Affiliated Hospital of Dalian Medical University
Lin Kang: The First Affiliated Hospital of Dalian Medical University
Yu Xu: The First Affiliated Hospital of Dalian Medical University
Liming Shen: The First Affiliated Hospital of Dalian Medical University
Shilin Jin: The First Affiliated Hospital of Dalian Medical University
Liang Wang: The First Affiliated Hospital of Dalian Medical University
Jing Liu: The First Affiliated Hospital of Dalian Medical University

Nature Communications, 2024, vol. 15, issue 1, 1-24

Abstract: Abstract Oxidative phosphorylation (OXPHOS) in the mitochondrial inner membrane is a therapeutic target in many diseases. Neural stem cells (NSCs) show progress in improving mitochondrial dysfunction in the central nervous system (CNS). However, translating neural stem cell-based therapies to the clinic is challenged by uncontrollable biological variability or heterogeneity, hindering uniform clinical safety and efficacy evaluations. We propose a systematic top-down design based on membrane self-assembly to develop neural stem cell-derived oxidative phosphorylating artificial organelles (SAOs) for targeting the central nervous system as an alternative to NSCs. We construct human conditionally immortal clone neural stem cells (iNSCs) as parent cells and use a streamlined closed operation system to prepare neural stem cell-derived highly homogenous oxidative phosphorylating artificial organelles. These artificial organelles act as biomimetic organelles to mimic respiration chain function and perform oxidative phosphorylation, thus improving ATP synthesis deficiency and rectifying excessive mitochondrial reactive oxygen species production. Conclusively, we provide a framework for a generalizable manufacturing procedure that opens promising prospects for disease treatment.

Date: 2024
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DOI: 10.1038/s41467-024-52171-2

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