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γPNAベースのmiR-122阻害剤によるミトコンドリアの停電の救助

Kamalika Mukherjee1, Suvendra N Bhattacharyya2

  • 1Department of Anesthesiology, University of Nebraska Medical Center, Omaha, NE 68198-4455, USA.

Molecular therapy. Nucleic acids
|February 24, 2026
PubMed
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No abstract available in PubMed .

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Energy to Drive Translocation01:37

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Mitochondrial protein import is powered by two distinct energy sources: ATP hydrolysis and electrochemical potential across the inner membrane. Newly synthesized precursors are bound by cytosolic chaperones of the Hsp70 family, which guide them to the import receptors on the mitochondrial surface. Utilizing the energy of ATP hydrolysis, Hsp70 chaperones transfer these precursors to the TOM receptors on the mitochondrial outer membrane.
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The mitochondrial electron transport chain (ETC) is the main energy generation system in the eukaryotic cells. However, mitochondria also produce cytotoxic reactive oxygen species (ROS) due to the large electron flow during oxidative phosphorylation. While Complex I is one of the primary sources of superoxide radicals, ROS production by Complex II is uncommon and may only be observed in cancer cells with mutated complexes.
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