Role of Mitochondrial Fission and Mitophagy in Parkinson's Disease

María F. Galindo, Maria E. Solesio, Joaquín Jordán

Research output: Chapter in Book/Report/Conference proceedingChapter

1 Scopus citations


The involvement of mitochondrial dysfunction as a causal factor of Parkinson's disease (PD) is well established. Impaired mitochondrial function is a predominant feature of PD. Here, we discuss mitochondrial fission and mitophagy, two processes that are described in PD. In experimental models as well as in samples from PD patients, mitochondrial fission has been shown to occur as an early step during these neurodegenerative processes. In these processes a machinery of proteins actively participates, including dynamin related protein 1 and fish. The deleterious effects of oxidative stress, resulting from increased levels of reactive oxygen species, including membrane and protein damage, are well recognized as important inducers of mitochondrial fission. Here, we discuss the current knowledge and prevailing hypotheses regarding mitochondrial dysfunction in either genetic or sporadic PD. While many questions remain unanswered, the prevalence of mitochondrial fission as an early event in neurodegenerative diseases warrants further exploration of all of these areas for development of potential treatments. Understanding the nature of these events, how they are activated, and their relative contributions to PD-mediated toxicity may strengthen future studies that aim to develop therapeutic prevention and intervention.

Original languageEnglish (US)
Title of host publicationMitophagy
PublisherElsevier Inc.
Number of pages13
ISBN (Electronic)9780124055339
ISBN (Print)9780124055285
StatePublished - Jul 25 2014
Externally publishedYes

All Science Journal Classification (ASJC) codes

  • Medicine(all)
  • Immunology and Microbiology(all)


  • Mitochondrial dynamics
  • Mitophagy in Parkinson's disease
  • PINK1
  • Parkin
  • Parkinson's disease
  • Sporadic PD
  • Sporadic Parkinson's disease


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