Restoration of mitochondrial function in cells with complex I deficiency

Yidong Bai, Jeong Soon Park, Jian Hong Deng, Youfen Li, Peiqing Hu

Research output: Contribution to journalArticle

11 Scopus citations

Abstract

The mammalian mitochondrial NADH dehydrogenase (complex I) is the major entry point for the electron transport chain. It is the largest and most complicated respiratory complex consisting of at least 46 subunits, 7 of which are encoded by mitochondrial DNA (mtDNA). Deficiency in complex I function has been associated with various human diseases including neurodegenerative diseases and the aging process. To explore ways to restore mitochondrial function in complex I-deficient cells, various cell models with mutations in genes encoding subunits for complex I have been established. In this paper, we discuss various approaches to recover mitochondrial activity, the complex I activity in particular, in cultured cells.

Original languageEnglish (US)
Pages (from-to)25-35
Number of pages11
JournalAnnals of the New York Academy of Sciences
Volume1042
DOIs
StatePublished - Jan 1 2005

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Keywords

  • Complex I deficiency
  • NDI1
  • Restoration
  • Revertant
  • mtDNA mutation

ASJC Scopus subject areas

  • Neuroscience(all)
  • Biochemistry, Genetics and Molecular Biology(all)
  • History and Philosophy of Science

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