Exploring the therapeutic potential of the mitochondrial transfer-associated enzymatic machinery in brain degeneration

Noymar Luque-Campos, Ricardo Riquelme, Luis Molina, Gisela Canedo-Marroquín, Ana María Vega-Letter, Patricia Luz-Crawford*, Felipe A. Bustamante-Barrientos*

*Corresponding author for this work

Research output: Contribution to journalReview articlepeer-review

2 Scopus citations


Mitochondrial dysfunction is a central event in the pathogenesis of several degenerative brain disorders. It entails fission and fusion dynamics disruption, progressive decline in mitochondrial clearance, and uncontrolled oxidative stress. Many therapeutic strategies have been formulated to reverse these alterations, including replacing damaged mitochondria with healthy ones. Spontaneous mitochondrial transfer is a naturally occurring process with different biological functions. It comprises mitochondrial donation from one cell to another, carried out through different pathways, such as the formation and stabilization of tunneling nanotubules and Gap junctions and the release of extracellular vesicles with mitochondrial cargoes. Even though many aspects of regulating these mechanisms still need to be discovered, some key enzymatic regulators have been identified. This review summarizes the current knowledge on mitochondrial dysfunction in different neurodegenerative disorders. Besides, we analyzed the usage of mitochondrial transfer as an endogenous revitalization tool, emphasizing the enzyme regulators that govern this mechanism. Going deeper into this matter would be helpful to take advantage of the therapeutic potential of mitochondrial transfer.

Original languageEnglish
Article number1217815
Pages (from-to)1-14
Number of pages14
JournalFrontiers in Physiology
StatePublished - 28 Jul 2023

Bibliographical note

Publisher Copyright:
Copyright © 2023 Luque-Campos, Riquelme, Molina, Canedo-Marroquín, Vega-Letter, Luz-Crawford and Bustamante-Barrientos.


  • cellular therapy
  • degenerative brain disorders
  • enzymes
  • fission and fusion
  • mitochondrial dysfunction
  • mitochondrial transfer
  • mitophagy
  • oxidative damage


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