Autophagy of Mitochondria: A Promising Therapeutic Target for Neurodegenerative Disease

Pradip K. Kamat, Anuradha Kalani, Philip Kyles, Suresh C. Tyagi, Neetu Tyagi

Research output: Contribution to journalReview articlepeer-review

43 Scopus citations

Abstract

The autophagic process is the only known mechanism for mitochondrial turnover and it has been speculated that dysfunction of autophagy may result in mitochondrial error and cellular stress. Emerging investigations have provided new understanding of how autophagy of mitochondria (also known as mitophagy) is associated with cellular oxidative stress and its impact on neurodegeneration. This impaired autophagic function may be considered as a possible mechanism in the pathogenesis of several neurodegenerative disorders including Parkinson’s disease, Alzheimer’s disease, multiple sclerosis, amyotrophic lateral sclerosis, and Huntington disease. It can be suggested that autophagy dysfunction along with oxidative stress is considered main events in neurodegenerative disorders. New therapeutic approaches have now begun to target mitochondria as a potential drug target. This review discusses evidence supporting the notion that oxidative stress and autophagy are intimately associated with neurodegenerative disease pathogenesis. This review also explores new approaches that can prevent mitochondrial dysfunction, improve neurodegenerative etiology, and also offer possible cures to the aforementioned neurodegenerative diseases.

Original languageEnglish (US)
Pages (from-to)707-719
Number of pages13
JournalCell Biochemistry and Biophysics
Volume70
Issue number2
DOIs
StatePublished - Oct 2 2014
Externally publishedYes

Keywords

  • Autophagy
  • Mitophagy
  • Neurodegeneration
  • Oxidative stress

ASJC Scopus subject areas

  • Biophysics
  • Biochemistry
  • Cell Biology

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