Mitophagy in neurodegeneration and aging
Open accessAbstract
Mitochondrial dysfunction contributes to normal aging and a wide spectrum of age-related diseases, including neurodegenerative disorders such as Parkinson's disease and Alzheimer's disease. It is important to maintain a healthy mitochondrial population which is tightly regulated by proteolysis and mitophagy. Mitophagy is a specialized form of autophagy that regulates the turnover of damaged and dysfunctional mitochondria, organelles that function in producing energy for the cell in the form of ATP and regulating energy homeostasis. Mechanistic studies on mitophagy across species highlight a sophisticated and integrated cellular network that regulates the degradation of mitochondria. Strategies directed at maintaining a healthy mitophagy level in aged individuals might have beneficial effects. In this review, we provide an updated mechanistic overview of mitophagy pathways and discuss the role of reduced mitophagy in neurodegeneration. We also highlight potential translational applications of mitophagy-inducing compounds, such as NAD+ precursors and urolithins.
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Mitophagy is inhibited in aging cells.
“Mitophagy, a specialized form of autophagy, which retards aging by removing mitochondrial fragments with activated mPTP, is also inhibited in aging cells”
From The mitochondrial permeability transition: Nexus of aging, disease and longevity (2021) · cites this paper as [160]
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- Authors
- Fivenson, E. M., Lautrup, S., Sun, N., Scheibye-Knudsen, M., Stevnsner, T., Nilsen, H., Bohr, V. A., & Fang, E. F.
- Affiliations
- National Institutes of Health (US)
- Aarhus University (DK)
- University of Oslo (NO)
- University of Copenhagen (DK)
- Corresponding author
- Bohr, Vilhelm A.
- Fang, Evandro F.
- ORCID
- Venue
- Neurochemistry International
- Publisher
- Elsevier BV
- Published
- 2017-10
- Volume
- 109
- Pages
- 202-209
- ISSN
- 0197-0186 (ISSN-L)
- PMC
- PMC5565781
- OpenAlex
- W2589775033
- Cited by
- 364
- References
- 110
- Citations by year
- 2026: 14 · 2025: 20 · 2024: 46 · 2023: 42 · 2022: 61 · 2021: 50 · 2020: 67 · 2019: 33 · 2018: 15 · 2017: 13 · 2016: 3
- FWCI
- 4.64
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Neurochemistry International (publishedVersion)
- PubMed (publishedVersion)
- Research at the University of Copenhagen (University of Copenhagen) (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Scopus (Elsevier) (submittedVersion)
- NORA - Norwegian Open Research Archives (submittedVersion, cc-by-nc-nd)
- Funders
- National Institute on Aging (EFF/VAB)
- Topics
- Health Sciences › Medicine › Epidemiology › Autophagy in Disease and Therapy
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
- Keywords
- mitophagy, neurodegeneration, aging, mitochondrial dysfunction, Parkinson's disease, Alzheimer's disease, autophagy, mitochondrial proteolysis, energy homeostasis, NAD+ precursors, urolithins
- MeSH terms
- Aging, Animals, Autophagy, Humans, Mitochondria, Neurodegenerative Diseases, Mitophagy
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