TY - JOUR
T1 - Role of Mitochondria–ER Contact Sites in Mitophagy
AU - Rühmkorf, Alina
AU - Harbauer, Angelika Bettina
N1 - Publisher Copyright:
© 2023 by the authors.
PY - 2023/8
Y1 - 2023/8
N2 - Mitochondria are often referred to as the “powerhouse” of the cell. However, this organelle has many more functions than simply satisfying the cells’ metabolic needs. Mitochondria are involved in calcium homeostasis and lipid metabolism, and they also regulate apoptotic processes. Many of these functions require contact with the ER, which is mediated by several tether proteins located on the respective organellar surfaces, enabling the formation of mitochondria–ER contact sites (MERCS). Upon damage, mitochondria produce reactive oxygen species (ROS) that can harm the surrounding cell. To circumvent toxicity and to maintain a functional pool of healthy organelles, damaged and excess mitochondria can be targeted for degradation via mitophagy, a form of selective autophagy. Defects in mitochondria–ER tethers and the accumulation of damaged mitochondria are found in several neurodegenerative diseases, including Parkinson’s disease and amyotrophic lateral sclerosis, which argues that the interplay between the two organelles is vital for neuronal health. This review provides an overview of the different mechanisms of mitochondrial quality control that are implicated with the different mitochondria–ER tether proteins, and also provides a novel perspective on how MERCS are involved in mediating mitophagy upon mitochondrial damage.
AB - Mitochondria are often referred to as the “powerhouse” of the cell. However, this organelle has many more functions than simply satisfying the cells’ metabolic needs. Mitochondria are involved in calcium homeostasis and lipid metabolism, and they also regulate apoptotic processes. Many of these functions require contact with the ER, which is mediated by several tether proteins located on the respective organellar surfaces, enabling the formation of mitochondria–ER contact sites (MERCS). Upon damage, mitochondria produce reactive oxygen species (ROS) that can harm the surrounding cell. To circumvent toxicity and to maintain a functional pool of healthy organelles, damaged and excess mitochondria can be targeted for degradation via mitophagy, a form of selective autophagy. Defects in mitochondria–ER tethers and the accumulation of damaged mitochondria are found in several neurodegenerative diseases, including Parkinson’s disease and amyotrophic lateral sclerosis, which argues that the interplay between the two organelles is vital for neuronal health. This review provides an overview of the different mechanisms of mitochondrial quality control that are implicated with the different mitochondria–ER tether proteins, and also provides a novel perspective on how MERCS are involved in mediating mitophagy upon mitochondrial damage.
KW - mitochondria
KW - mitophagy
KW - organellar contact sites
UR - http://www.scopus.com/inward/record.url?scp=85168748519&partnerID=8YFLogxK
U2 - 10.3390/biom13081198
DO - 10.3390/biom13081198
M3 - Review article
C2 - 37627263
AN - SCOPUS:85168748519
SN - 2218-273X
VL - 13
JO - Biomolecules
JF - Biomolecules
IS - 8
M1 - 1198
ER -