Role of Mitochondria-ER Contact Sites in Mitophagy.


Journal

Biomolecules
ISSN: 2218-273X
Titre abrégé: Biomolecules
Pays: Switzerland
ID NLM: 101596414

Informations de publication

Date de publication:
31 07 2023
Historique:
received: 30 06 2023
revised: 28 07 2023
accepted: 29 07 2023
medline: 28 8 2023
pubmed: 26 8 2023
entrez: 26 8 2023
Statut: epublish

Résumé

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.

Identifiants

pubmed: 37627263
pii: biom13081198
doi: 10.3390/biom13081198
pmc: PMC10452924
pii:
doi:

Substances chimiques

Mitochondrial Proteins 0
Receptors, Estrogen 0

Types de publication

Journal Article Review Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Déclaration de conflit d'intérêts

The authors declare no conflict of interest.

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Auteurs

Alina Rühmkorf (A)

TUM Medical Graduate Center, Technical University of Munich, 81675 Munich, Germany.
Max Planck Institute for Biological Intelligence, 82152 Planegg-Martinsried, Germany.

Angelika Bettina Harbauer (AB)

Max Planck Institute for Biological Intelligence, 82152 Planegg-Martinsried, Germany.
Institute of Neuronal Cell Biology, Technical University of Munich, 80802 Munich, Germany.
Munich Cluster for Systems Neurology, 81377 Munich, Germany.

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