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Mitochondrial DNA damage and atherosclerosis
Open accessAbstract
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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“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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Lood, C., Blanco, L. P., Purmalek, M. M., Carmona-Rivera, C., De Ravin, S. S., Smith, C. K., Malech, H. L., Ledbetter, J. A., Elkon, K. B., & Kaplan, M. J. (2016) · Nature Medicine · doi:10.1038/nm.4027 · Cited by 1,570
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“Interaction of TLR9 with mtDNA activates the nuclear factor kappa B (NF-j B) signaling and increases the expression of other pro-inflammatory cytokines such as tumor necrosis factor-a (TNF-a ), interleukin (IL)-6, IL-1 b (Julian et al , 2013; Yu & Bennett, 2014; Zhang et al , 2014).”
Metadata
- 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
- Licence
- cc-by-nc-nd
- www.elsevier.com/tdm/userlicense/1.0/ (tdm)
- 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
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › 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
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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