| Literature DB >> 28235551 |
Elayne M Fivenson1, Sofie Lautrup2, Nuo Sun3, Morten Scheibye-Knudsen4, Tinna Stevnsner5, Hilde Nilsen6, Vilhelm A Bohr7, Evandro F Fang8.
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. Published by Elsevier Ltd.Entities:
Mesh：
Year: 2017 PMID： 28235551 PMCID： PMC5565781 DOI： 10.1016/j.neuint.2017.02.007
Source DB: PubMed Journal: Neurochem Int ISSN： 0197-0186 Impact factor: 3.921