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Targeting the Mitochondrial Permeability Transition Pore to Prevent Age-Associated Cell Damage and Neurodegeneration

Oxidative medicine and cellular longevity, 2021, Vol.2021, p.6626484-15 [Peer Reviewed Journal]

Copyright © 2021 Andrew C. Kent et al. ;Copyright © 2021 Andrew C. Kent et al. This is an open access article distributed under the Creative Commons Attribution License (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. https://creativecommons.org/licenses/by/4.0 ;Copyright © 2021 Andrew C. Kent et al. 2021 ;ISSN: 1942-0900 ;EISSN: 1942-0994 ;DOI: 10.1155/2021/6626484 ;PMID: 33574977

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  • Title:
    Targeting the Mitochondrial Permeability Transition Pore to Prevent Age-Associated Cell Damage and Neurodegeneration
  • Author: Kent, Andrew C. ; El Baradie, Khairat Bahgat Youssef ; Hamrick, Mark W.
  • Biundo, Fabrizio ; Fabrizio Biundo
  • Subjects: Age ; Aging ; Aging - pathology ; Animals ; Humans ; Mitochondria ; Mitochondrial Permeability Transition Pore - chemistry ; Mitochondrial Permeability Transition Pore - metabolism ; Models, Biological ; Mutagenesis ; Nerve Degeneration - pathology ; Oxidative stress ; Permeability ; Proteins ; Reactive Oxygen Species - metabolism ; Respiration ; Review
  • Is Part Of: Oxidative medicine and cellular longevity, 2021, Vol.2021, p.6626484-15
  • Description: The aging process is associated with significant alterations in mitochondrial function. These changes in mitochondrial function are thought to involve increased production of reactive oxygen species (ROS), which over time contribute to cell death, senescence, tissue degeneration, and impaired tissue repair. The mitochondrial permeability transition pore (mPTP) is likely to play a critical role in these processes, as increased ROS activates mPTP opening, which further increases ROS production. Injury and inflammation are also thought to increase mPTP opening, and chronic, low-grade inflammation is a hallmark of aging. Nicotinamide adenine dinucleotide (NAD+) can suppress the frequency and duration of mPTP opening; however, NAD+ levels are known to decline with age, further stimulating mPTP opening and increasing ROS release. Research on neurodegenerative diseases, particularly on Parkinson’s disease (PD) and Alzheimer’s disease (AD), has uncovered significant findings regarding mPTP openings and aging. Parkinson’s disease is associated with a reduction in mitochondrial complex I activity and increased oxidative damage of DNA, both of which are linked to mPTP opening and subsequent ROS release. Similarly, AD is associated with increased mPTP openings, as evidenced by amyloid-beta (Aβ) interaction with the pore regulator cyclophilin D (CypD). Targeted therapies that can reduce the frequency and duration of mPTP opening may therefore have the potential to prevent age-related declines in cell and tissue function in various systems including the central nervous system.
  • Publisher: United States: Hindawi
  • Language: English
  • Identifier: ISSN: 1942-0900
    EISSN: 1942-0994
    DOI: 10.1155/2021/6626484
    PMID: 33574977
  • Source: MEDLINE
    PubMed Central
    Alma/SFX Local Collection
    ProQuest Central
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