Activation of transcription factor Nrf2 to counteract mitochondrial dysfunction in Parkinson’s disease

Claudia Bento-Pereira, Albena Dinkova-Kostova (Lead / Corresponding author)

Research output: Contribution to journalReview articlepeer-review

41 Citations (Scopus)
119 Downloads (Pure)


Parkinson's disease (PD) is a progressive neurodegenerative disorder, for which no disease-modifying therapies are available to date. Although understanding of the precise aetiology of PD is incomplete, it is clear that age, genetic predisposition and environmental stressors increase the risk. At the cellular level, oxidative stress, chronic neuroinflammation, mitochondrial dysfunction and aberrant protein aggregation have been implicated as contributing factors. These detrimental processes are counteracted by elaborate networks of cellular defence mechanisms, one of which is orchestrated by transcription factor nuclear factor-erythroid 2 p45-related factor 2 (Nrf2; gene name NFE2L2). A wealth of preclinical evidence suggests that Nrf2 activation is beneficial in cellular and animal models of PD. In this review, we summarise the current understanding of mitochondrial dysfunction in PD, the role of Nrf2 in mitochondrial function and explore the potential of Nrf2 as a therapeutic target for mitochondrial dysfunction in PD.

Original languageEnglish
Pages (from-to)785-802
Number of pages18
JournalMedicinal Research Reviews
Issue number2
Early online date18 Jul 2020
Publication statusPublished - 25 Feb 2021


  • Nrf2
  • Parkinson's disease
  • oxidative stress

ASJC Scopus subject areas

  • Molecular Medicine
  • Pharmacology
  • Drug Discovery


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