Cited by 124Mitochondrial Function and PathologyAtherosclerosis and Cardiovascular DiseasesAutophagy in Disease and Therapy

Mitochondrial DNA damage and atherosclerosis

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Yu, Emma P.K., Bennett, Martin R.·2014·Trends in Endocrinology & Metabolism

Abstract

Mitochondria are often regarded as the cellular powerhouses through their ability to generate ATP, the universal fuel for metabolic processes. However, in recent years mitochondria have been recognised as critical regulators of cell death, inflammation, metabolism, and the generation of reactive oxygen species (ROS). Thus, mitochondrial dysfunction directly promotes cell death, inflammation, and oxidative stress and alters metabolism. These are key processes in atherosclerosis and there is now evidence that mitochondrial DNA (mtDNA) damage leads to mitochondrial dysfunction and promotes atherosclerosis directly. In this review we discuss the recent evidence for and mechanisms linking mtDNA defects and atherosclerosis and suggest areas of mitochondrial biology that are potential therapeutic targets.

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Crossref · 10.1016/j.tem.2014.06.008

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  • TLR9 interaction with mtDNA activates NF-kB signaling and increases pro-inflammatory cytokine expression.

    “Interaction of TLR9 with mtDNA activates the nuclear factor kappa B (NF-jB) signaling and increases the expression of other pro-inflammatory cytokines such as tumor necrosis factor-a (TNF-a), interleukin (IL)-6, IL-1b (Julian et al, 2013;Yu & Bennett, 2014;Zhang et al, 2014).”

    From Mitochondrial DNA and TLR9 drive muscle inflammation upon Opa1 deficiency (2018) · cites this paper as Yu & Bennett, 2014

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Authors
Yu, E. P. K., & Bennett, M. R.
Affiliations
University of Cambridge (GB)
Corresponding author
Yu, Emma P.K.
Venue
Trends in Endocrinology & Metabolism
Publisher
Elsevier BV
Published
2014-09
Volume
25
Issue
9
Pages
481-487
ISSN
1043-2760 (ISSN-L)
OpenAlex
W2047242190
Cited by
124
References
64
Citations by year
2026: 8 · 2025: 8 · 2024: 6 · 2023: 7 · 2022: 8 · 2021: 14 · 2020: 20 · 2019: 13 · 2018: 11 · 2017: 9 · 2016: 11 · 2015: 7 · 2014: 2
FWCI
0.91
Type
journal article
Language
en
Open access
Locations
  • Trends in Endocrinology and Metabolism (publishedVersion)
  • PubMed (publishedVersion)
  • Apollo (University of Cambridge) (acceptedVersion, cc-by-nc-nd)
  • Apollo (University of Cambridge) (submittedVersion)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
  • Life Sciences › Immunology and Microbiology › Immunology › Atherosclerosis and Cardiovascular Diseases
  • Health Sciences › Medicine › Epidemiology › Autophagy in Disease and Therapy
Keywords
mitochondrial DNA damage, atherosclerosis, mitochondrial dysfunction, reactive oxygen species, oxidative stress, inflammation, cell death, metabolism, therapeutic target
MeSH terms
Animals, DNA Damage, DNA, Mitochondrial, Humans, Models, Biological, Apoptosis, Oxidative Stress, Atherosclerosis, Mitochondrial Dynamics

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