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 remain
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.
Author(s):
Catherine E Rodger, Thomas G McWilliams, Ian G Ganley
PubMed:
29151277
Citation:
Catherine E Rodger, Thomas G McWilliams, Ian G Ganley
Catherine E Rodger, Thomas G McWilliams, Ian G Ganley
The FEBS journal
2018
285 (7)
1185-1202
PMID: 29151277