Journal
MOLECULAR BIOLOGY REPORTS
Volume 49, Issue 11, Pages 10749-10760Publisher
SPRINGER
DOI: 10.1007/s11033-022-07738-x
Keywords
Mitophagy; PINK1; Parkin; NIX; BNIP3L; FUNDC1; Neurodegenerative diseases
Categories
Funding
- National Natural Science Foundation of China [32171131, 82071429]
- Shandong Province Natural Science Foundation [2021ZDSYS11, ZR2019ZD31, ZR2020MC072]
- Innovative Research Team of High-Level Local Universities in Shanghai
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Mitochondrial dysfunction and impaired mitophagy play significant roles in neurodegenerative diseases, and modulation of mitophagy may serve as a therapeutic strategy for these diseases.
Mitochondria dysfunction has been defined as one of the hallmarks of aging-related diseases as is characterized by the destroyed integrity, abnormal distribution and size, insufficient ATP supply, increased ROS production, and subsequently damage and oxidize the proteins, lipids and nucleic acid. Mitophagy, an efficient way of removing damaged or defective mitochondria by autophagy, plays a pivotal role in maintaining the mitochondrial quantity and quality control enabling the degradation of unwanted mitochondria, and thus rescues cellular homeostasis in response to stress. Accumulating evidence demonstrates that impaired mitophagy has been associated with many neurodegenerative diseases, such as Alzheimer's disease (AD), Parkinson's disease (PD) and Huntington's disease (HD), amyotrophic lateral sclerosis (ALS) in a variety of patients and disease models with neural death, oxidative stress and disturbed metabolism, either as the cause or consequence. These findings suggest that modulation of mitophagy may be considered as a valid therapeutic strategy in neurodegenerative diseases. In this review, we summarize recent findings on the mechanisms of mitophagy and its role in neurodegenerative diseases, with a particular focus on mitochondrial proteins acting as receptors that mediate mitophagy in these diseases.
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