Cited by 364Autophagy in Disease and TherapyMitochondrial Function and PathologyGenetics, Aging, and Longevity in Model Organisms

Mitophagy in neurodegeneration and aging

Open access
Fivenson, Elayne M., Lautrup, Sofie, Sun, Nuo, Scheibye-Knudsen, Morten, Stevnsner, Tinna, Nilsen, Hilde, Bohr, Vilhelm A., Fang, Evandro F.·2017·Neurochemistry International

Abstract

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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  1. [61]Palikaras K Lionaki E Tavernarakis N Coordination of mitophagy and mitochondrial biogenesis during ageing in C. elegans Nature 2015 521 7553 525 528 25896323
  2. [93]Fang EF Nuclear DNA damage signalling to mitochondria in ageing Nature Reviews Molecular Cell Biology 2016 17 5 308 321 26956196 PMC5161407
  3. [99]Fang EF Defective mitophagy in XPA via PARP-1 hyperactivation and NAD+/SIRT1 reduction Cell 2014 157 4 882 896 24813611 PMC4625837
  4. [100]Fang EF NAD+ Replenishment Improves Lifespan and Healthspan in Ataxia Telangiectasia Models via Mitophagy and DNA Repair Cell metabolism 2016 24 4 566 581 27732836 PMC5777858

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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.
Venue
Neurochemistry International
Publisher
Elsevier BV
Published
2017-10
Volume
109
Pages
202-209
ISSN
0197-0186 (ISSN-L)
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
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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