Mammalian mitophagy – from in vitro molecules to in vivo models

Catherine E. Rodger, Thomas G. McWilliams, Ian G. Ganley (Lead / Corresponding author)

Research output: Contribution to journalReview articlepeer-review

98 Citations (Scopus)
216 Downloads (Pure)

Abstract

The autophagic turnover of mitochondria, termed mitophagy, is thought to play an essential role in not only maintaining the health of the mitochondrial network, but also that of the cell and organism as a whole. We have come a long way in identifying the molecular components required for mitophagy through extensive in vitro work and cell line characterisation, yet the physiological significance and context of these pathways remains largely unexplored. This is highlighted by the recent development of new mouse models that have revealed a striking level of variation in mitophagy, even under normal conditions. Here we focus on programmed mitophagy and summarise our current understanding of why, how and where this takes place in mammals.
Original languageEnglish
Pages (from-to)1185-1202
Number of pages18
JournalFEBS Journal
Volume285
Issue number7
Early online date19 Nov 2017
DOIs
Publication statusPublished - Apr 2018

Keywords

  • Autophagy
  • Metabolism
  • Mitochondria
  • Mitophagy
  • NIX
  • Parkin
  • PINK1
  • ULK1
  • Mito-QC
  • Mouse models
  • Development
  • Disease

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