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MtDNA deletions and aging

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MtDNA deletions and aging. / Sprason, Charlotte; Tucker, Trudy; Clancy, David.
In: Frontiers in Aging, Vol. 5, 1359638, 15.02.2024.

Research output: Contribution to Journal/MagazineReview articlepeer-review

Harvard

Sprason, C, Tucker, T & Clancy, D 2024, 'MtDNA deletions and aging', Frontiers in Aging, vol. 5, 1359638. https://doi.org/10.3389/fragi.2024.1359638

APA

Sprason, C., Tucker, T., & Clancy, D. (2024). MtDNA deletions and aging. Frontiers in Aging, 5, Article 1359638. https://doi.org/10.3389/fragi.2024.1359638

Vancouver

Sprason C, Tucker T, Clancy D. MtDNA deletions and aging. Frontiers in Aging. 2024 Feb 15;5:1359638. doi: 10.3389/fragi.2024.1359638

Author

Sprason, Charlotte ; Tucker, Trudy ; Clancy, David. / MtDNA deletions and aging. In: Frontiers in Aging. 2024 ; Vol. 5.

Bibtex

@article{b3ce81388801454c8b6a326f04b8bcd5,
title = "MtDNA deletions and aging",
abstract = "Aging is the major risk factor in most of the leading causes of mortality worldwide, yet its fundamental causes mostly remain unclear. One of the clear hallmarks of aging is mitochondrial dysfunction. Mitochondria are best known for their roles in cellular energy generation, but they are also critical biosynthetic and signaling organelles. They also undergo multiple changes with organismal age, including increased genetic errors in their independent, circular genome. A key group of studies looking at mice with increased mtDNA mutations showed that premature aging phenotypes correlated with increased deletions but not point mutations. This generated an interest in mitochondrial deletions as a potential fundamental cause of aging. However, subsequent studies in different models have yielded diverse results. This review summarizes the research on mitochondrial deletions in various organisms to understand their possible roles in causing aging while identifying the key complications in quantifying deletions across all models.",
keywords = "aging, mitochondria, mitochondrial DNA deletions, mitochondrial dysfunction, mitochondrial DNA",
author = "Charlotte Sprason and Trudy Tucker and David Clancy",
year = "2024",
month = feb,
day = "15",
doi = "10.3389/fragi.2024.1359638",
language = "English",
volume = "5",
journal = "Frontiers in Aging",
issn = "2673-6217",
publisher = "Frontiers Media S.A.",

}

RIS

TY - JOUR

T1 - MtDNA deletions and aging

AU - Sprason, Charlotte

AU - Tucker, Trudy

AU - Clancy, David

PY - 2024/2/15

Y1 - 2024/2/15

N2 - Aging is the major risk factor in most of the leading causes of mortality worldwide, yet its fundamental causes mostly remain unclear. One of the clear hallmarks of aging is mitochondrial dysfunction. Mitochondria are best known for their roles in cellular energy generation, but they are also critical biosynthetic and signaling organelles. They also undergo multiple changes with organismal age, including increased genetic errors in their independent, circular genome. A key group of studies looking at mice with increased mtDNA mutations showed that premature aging phenotypes correlated with increased deletions but not point mutations. This generated an interest in mitochondrial deletions as a potential fundamental cause of aging. However, subsequent studies in different models have yielded diverse results. This review summarizes the research on mitochondrial deletions in various organisms to understand their possible roles in causing aging while identifying the key complications in quantifying deletions across all models.

AB - Aging is the major risk factor in most of the leading causes of mortality worldwide, yet its fundamental causes mostly remain unclear. One of the clear hallmarks of aging is mitochondrial dysfunction. Mitochondria are best known for their roles in cellular energy generation, but they are also critical biosynthetic and signaling organelles. They also undergo multiple changes with organismal age, including increased genetic errors in their independent, circular genome. A key group of studies looking at mice with increased mtDNA mutations showed that premature aging phenotypes correlated with increased deletions but not point mutations. This generated an interest in mitochondrial deletions as a potential fundamental cause of aging. However, subsequent studies in different models have yielded diverse results. This review summarizes the research on mitochondrial deletions in various organisms to understand their possible roles in causing aging while identifying the key complications in quantifying deletions across all models.

KW - aging

KW - mitochondria

KW - mitochondrial DNA deletions

KW - mitochondrial dysfunction

KW - mitochondrial DNA

U2 - 10.3389/fragi.2024.1359638

DO - 10.3389/fragi.2024.1359638

M3 - Review article

VL - 5

JO - Frontiers in Aging

JF - Frontiers in Aging

SN - 2673-6217

M1 - 1359638

ER -