Targeting mitochondrial calcium pathways as a potential treatment against Parkinson's disease

Kuntal Dey, Michal A. Bazala, Jacek Kuznicki

Research output: Contribution to journalArticlepeer-review

24 Scopus citations


Parkinson's disease (PD) is a major health problem worldwide affecting millions of people and is a result of neurodegeneration in a small part of the brain known as substantia nigra pars compacta. Aberration in mitochondrial Ca2+ homeostasis plays, among several other factors, an important role for the neuronal loss in PD. Mitochondria are vital for cellular physiology, e.g. for ATP generation, and mitochondrial Ca2+ is a key player in cell functioning and survival. Mitochondrial Ca2+ homeostasis is maintained by a fine balance between the activities of proteins mediating the influx and efflux of Ca2+ across mitochondrial membranes. Malfunctioning of these proteins leading to Ca2+ overload promotes ROS generation, which induces cell death by triggering the opening of mitochondrial permeability transition pore. Till now PD remains incurable and the “gold standard” drug which can only delays the disease progression is L-Dopa from the 1960s and therefore, the situation warrants the search for novel targets for the treatment of the PD patients. In this review, we summarize the current views that suggest mitochondrial Ca2+ regulatory pathways are good candidates for the treatment of PD.

Original languageEnglish
Article number102216
JournalCell Calcium
StatePublished - 1 Jul 2020
Externally publishedYes


  • Ca
  • MCU
  • Mitochondria
  • NCLX
  • Parkinson's disease
  • VDAC

ASJC Scopus subject areas

  • Physiology
  • Molecular Biology
  • Cell Biology


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