Hello. My name is Anna Vainshtein.
I'm the CEO and founder of Craft Science Inc.,
a scientific writing, editing,
and consulting firm based out of Toronto, Canada.
Today, I'll be talking to you about the role of mitophagy,
which is the degradation of
dysfunctional and superfluous organelles in mitochondrial quality control.
This talk, will focus on
five major themes including mitochondrial function and dysfunction,
the mechanisms of mitochondrial quality control.
I will then briefly introduce autophagy as
the core autophagy machinery is required for mitophagy.
I will also describe the mechanisms of mitophagy and finally,
the physiological and pathological roles of this process.
Mitochondria constitute the main energy-producing centers of eukaryotic cells,
and so-called power plants of the cell.
But in addition, they are also involved in several crucial cellular processes.
In healthy cells, these functions are highly regulated to
provide sufficient energy for cell functions,
maintain cell homeostasis, and avoid undesirable cell death.
Aside from ATP production,
mitochondria also play an important role in calcium storage and uptake,
produce reactive oxygen species or ROS as a byproduct of oxidative phosphorylation.
Mitochondria are also the principal source of a Acetyl-CoA, and if permeablized,
can release internal factors that can act as death signals such as Cytochrome c. Indeed,
changes in cellular ATP can dictate organelle
trafficking from one area of the cell to another,
based on energy needs.
While changes in mitochondrial calcium buffering capacity and
reactive oxygen species production may activate signaling pathways,
they can determine cellular growth and protein synthesis.
While alterations in Acetyl-CoA levels can lead to
chromatin remodeling mediated by
histone acetyltransferases and this changes to gene transcription.
While mitochondria damage or increased
cellular stress can result in the release of mitochondrial factors,
such as Cytochrome c, which can lead to programmed cell death known as apoptosis.
It is therefore vital to maintain mitochondrial health and vitality.
As a byproduct of oxidative phosphorylation,