Role of Mitochondria–ER Contact Sites in Mitophagy
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 func...
| Main Authors: | , |
|---|---|
| Format: | Article |
| Language: | English |
| Published: |
MDPI AG
2023-07-01
|
| Series: | Biomolecules |
| Subjects: | |
| Online Access: | https://www.mdpi.com/2218-273X/13/8/1198 |
| _version_ | 1797585425854889984 |
|---|---|
| author | Alina Rühmkorf Angelika Bettina Harbauer |
| author_facet | Alina Rühmkorf Angelika Bettina Harbauer |
| author_sort | Alina Rühmkorf |
| collection | DOAJ |
| description | 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. |
| first_indexed | 2024-03-11T00:05:56Z |
| format | Article |
| id | doaj.art-f6c24ef22c1d44c6826f7fb2c81e4599 |
| institution | Directory Open Access Journal |
| issn | 2218-273X |
| language | English |
| last_indexed | 2024-03-11T00:05:56Z |
| publishDate | 2023-07-01 |
| publisher | MDPI AG |
| record_format | Article |
| series | Biomolecules |
| spelling | doaj.art-f6c24ef22c1d44c6826f7fb2c81e45992023-11-19T00:23:37ZengMDPI AGBiomolecules2218-273X2023-07-01138119810.3390/biom13081198Role of Mitochondria–ER Contact Sites in MitophagyAlina Rühmkorf0Angelika Bettina Harbauer1TUM Medical Graduate Center, Technical University of Munich, 81675 Munich, GermanyMax Planck Institute for Biological Intelligence, 82152 Planegg-Martinsried, GermanyMitochondria 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.https://www.mdpi.com/2218-273X/13/8/1198mitochondriamitophagyorganellar contact sites |
| spellingShingle | Alina Rühmkorf Angelika Bettina Harbauer Role of Mitochondria–ER Contact Sites in Mitophagy Biomolecules mitochondria mitophagy organellar contact sites |
| title | Role of Mitochondria–ER Contact Sites in Mitophagy |
| title_full | Role of Mitochondria–ER Contact Sites in Mitophagy |
| title_fullStr | Role of Mitochondria–ER Contact Sites in Mitophagy |
| title_full_unstemmed | Role of Mitochondria–ER Contact Sites in Mitophagy |
| title_short | Role of Mitochondria–ER Contact Sites in Mitophagy |
| title_sort | role of mitochondria er contact sites in mitophagy |
| topic | mitochondria mitophagy organellar contact sites |
| url | https://www.mdpi.com/2218-273X/13/8/1198 |
| work_keys_str_mv | AT alinaruhmkorf roleofmitochondriaercontactsitesinmitophagy AT angelikabettinaharbauer roleofmitochondriaercontactsitesinmitophagy |