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

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Mitochondrial DNA damage and atherosclerosis

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

DOI 10.1016/j.tem.2014.06.008

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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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Mediating effects of platelet-derived extracellular vesicles on PM2.5-induced vascular endothelial injury
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“Mitochondrial damage promotes the release of mtDNA into the cytoplasm, consequently activating NLRP3 inflammasome and upregulating IL-1β and IL-18 inflammatory factors by caspase-1 [43, 44].”
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“The accumulating global data on the mtDNA damage in atherosclerosis [62,63] make this hypothesis plausible, taking in account the role of increased oxidative stress as the mechanistic factor of atherosclerotic risk.”
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Carbonyl cyanide 3-chlorophenylhydrazone induced the imbalance of mitochondrial homeostasis in the liver of Megalobrama amblycephala: A dynamic study
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“Thus, mitochondria are often targeted for bacterial attack and show functional abnormalities, including mitochondrial reactive oxygen species (mtROS)-induced oxidative stress, mitochondrial DNA (mtDNA) mutation and release, and imbalance of mitochondrial dynamics, further contributing to arterial wall cell damage, inf…”
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Trimetazidine Protects Against Atherosclerosis by Changing Energy Charge and Oxidative Stress
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“Recent studies suggested that the development of atherosclerosis is also accompanied by energy depletion [9,10].”
Background
Lack of mitochondrial NADP(H)-transhydrogenase expression in macrophages exacerbates atherosclerosis in hypercholesterolemic mice
Salerno, A. G., Rentz, T., Dorighello, G. G., Marques, A. C., Lorza‐Gil, E., Wanschel, A. C. B. A., de Moraes, A., Vercesi, A. E., & Oliveira, H. C. F. (2019) · Biochemical Journal · doi:10.1042/bcj20190543 · Cited by 21
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Grape seed proanthocyanidins prevent H 2 O 2 ‐induced mitochondrial dysfunction and apoptosis via SIRT 1 activation in embryonic kidney cells
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“Повреждения митохондриальной ДНК Помимо мутаций в ядерной ДНК одним из ранних звеньев патогенеза атеросклероза являются мутации митохондриальной ДНК (мтДНК) [53-56].”
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“Plaque vulnerability is further promoted by mtDNA defects via monocyte cell death and the resultant increased release of inflammatory cytokine.(38) From these studies, it can be seen that mitochondrial dysfunction, possibly as a result of mtDNA variants or damage, can directly be implicated in mechanisms that encumber…”
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CISD1 protects against atherosclerosis by suppressing lipid accumulation and inflammation via mediating Drp1
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“In addition, several studies have demonstrated that mutations in mitochondrial DNA (mtDNA) are associated with key features of atherosclerosis, including inflammation and oxidative stress [6].”
Background
Adaptation of mitochondrial expression and ATP production in dedifferentiating vascular smooth muscle cells
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Studies of the Formation and Stability of Ezetimibe-Cyclodextrin Inclusion Complexes
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Upregulation of ALOX12−12-HETE pathway impairs AMPK-dependent modulation of vascular metabolism in ApoE/LDLR−/− mice
Olkowicz, M., Karaś, A., Berkowicz, P., Kaczara, P., Jasztal, A., Kuryłowicz, Z., Fedak, F. A., Rosales-Solano, H., Roy, K. S., Kij, A., et al. (2024) · Pharmacological Research · doi:10.1016/j.phrs.2024.107478 · Cited by 18
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Metabolic Strategies in Healthcare: A New Era
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“First, it does not sufficiently address the striking oxidative damage and mitochondria dysfunction observed in human plaques [13,14].”
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Hefti, E., & Blanco, J. G. (2017) · Mitochondrial DNA Part A · doi:10.1080/24701394.2017.1325480 · Cited by 15
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High-Fat and Combined High-Fat and Sucrose Diets Promote Cardiac Oxidative Stress Independent of Nox2 Redox Regulation and Obesity in Rats
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Background

Authors: Yu, E. P. K., & Bennett, M. R.
Affiliations: University of Cambridge (GB)
Corresponding author: Yu, Emma P.K.
ORCID: Yu, Emma P.K.
Bennett, Martin R.
Venue: Trends in Endocrinology & Metabolism
Publisher: Elsevier BV
Published: 2014-09
Volume: 25
Issue: 9
Pages: 481-487
ISSN: 1043-2760 (ISSN-L)
DOI: 10.1016/j.tem.2014.06.008
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: green
www.repository.cam.ac.uk
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

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