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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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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Mitochondria as a target for neuroprotection: role of methylene blue and photobiomodulation
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Mitochondrial metabolism and the control of vascular smooth muscle cell proliferation
Chiong, M., Cartes-Saavedra, B., Norambuena‐Soto, I., Mondaca‐Ruff, D., Morales, P. E., García-Miguel, M., & Mellado, R. (2014) · Frontiers in Cell and Developmental Biology · doi:10.3389/fcell.2014.00072 · Cited by 137 · see citing works
“Mitochondria has four compartments: the outer mitochondrial membrane (OMM), the intermembrane space (IMS), the inner mitochondrial membrane (IMM), and the mitochondrial matrix (Scheffler, 2001).”
BackgroundHu, Q., Shi, H., Zeng, T., Liu, H., Su, Y., Cheng, X., Ye, J., Yin, Y., Liu, M., Zheng, H. W., et al. (2019) · Arthritis Research & Therapy · doi:10.1186/s13075-018-1800-z · Cited by 134 · see citing works
The sensing of mitochondrial DAMPs by non-immune cells
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“Several studies have reported the relevance of circulating or extracellular mtDNA in TLR9dependent inflammation in diseases such as rheumatoid arthritis [122], atherosclerosis [10, 123], acute liver injury [71], and Streptococcus pneumoniae infections [124], among others [10, 62, 125–129].”
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“Damage to mitochondrial DNA has been shown to mediate mitochondrial dysfunction including alterations in calcium handling, oxidant-mediated activation of cell stress pathways, and metabolic disturbances [5, 11, 12, 18].”
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“islands.(20) Given that mtDNA lacks the repair proteins and protective histones found in nuclear DNA (nDNA), mtDNA is more easily attacked by reactive oxygen species (ROS),(21,22) which are byproducts of mitochondrial respiration.”
BackgroundSleep and biological aging: A short review
Carroll, J., & Prather, A. A. (2021) · Current Opinion in Endocrine and Metabolic Research · doi:10.1016/j.coemr.2021.03.021 · Cited by 93 · see citing works
The role of mitochondrial DNA damage in the development of atherosclerosis
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Self-citationPM2.5 aggravates the lipid accumulation, mitochondrial damage and apoptosis in macrophage foam cells
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Mitochondrial Dysfunction in Vascular Wall Cells and Its Role in Atherosclerosis
Salnikova, D. I., Orekhova, V. A., Grechko, A. V., Starodubova, A. V., Bezsonov, E. E., Попкова, Т. В., & Orekhov, A. N. (2021) · International Journal of Molecular Sciences · doi:10.3390/ijms22168990 · Cited by 84 · see citing works
“Mitochondrial oxidative stress can exacerbate mitochondrial dysfunction by damaging mtDNA and organelle structures therefore forming a vicious cycle [14,16].”
BackgroundMitochondrial Dysfunction in Cardiovascular Diseases
Yang, H. (2025) · International Journal of Molecular Sciences · doi:10.3390/ijms26051917 · Cited by 86 · see citing works
“Elevated ROS levels in atherosclerotic plaques have been linked to increased oxidative stress and inflammation [83].”
Zhang, L., Deng, S., Zhao, S., Ai, Y., Zhang, L., Pan, P., Su, X., Tan, H., & Wu, D. (2016) · International Journal of Molecular Sciences · doi:10.3390/ijms17091425 · Cited by 78 · see citing works
“MtDNA, similar to that of its bacterial ancestors, consists of a circular loop and contains a significant amount of un-methylated DNA present as CpG islands [14].”
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PCSK9: A novel inflammation modulator in atherosclerosis?
Tang, Z., Li, T., Peng, J., Zheng, J., Li, T., Liu, L., Jiang, Z., & Zheng, X. (2018) · Journal of Cellular Physiology · doi:10.1002/jcp.27254 · Cited by 73 · see citing works
“A positive bi‐directional interaction was demonstrated between PCSK9 and mitochondrial DNA (mtDNA) damage in VSMCs treated with LPS (Ding et al., 2016). mtDNA damage leads to inflammation, oxidative stress, and apoptosis, which directly contribute to atherosclerosis (Yu & Bennett, 2014, 2016).”
BackgroundProtective Mechanisms of Mitochondria and Heart Function in Diabetes
Aon, M. A., Tocchetti, C. G., Bhatt, N., Paolocci, N., & Cortassa, S. C. (2015) · Antioxidants and Redox Signaling · doi:10.1089/ars.2014.6123 · Cited by 70 · see citing works
“Another important mechanism of hyperglycemic damage involves alterations in mitochondrial DNA (mtDNA) that encodes 37 genes, among them 13 essential OxPhos components (198), thus potentially causing energetic failure and contributing to atherosclerosis (215).”
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“MtDNA content decrease leads to excess mitochondrial ROS production and subsequently causes transactivation of proatherogenic genes such as plasminogen activator inhibitor-1 (PAI-1), transforming growth factor b1(TGF-b1), vascular cell adhesion molecule-1 (VCAM-1) and monocyte chemoattractant protein-1 (MCP-1), sugges…”
BackgroundResearch progress on the pharmacological effects of berberine targeting mitochondria
Fang, X., Wu, H., Wei, J., Miao, R., Zhang, Y., & Tian, J. (2022) · Frontiers in Endocrinology · doi:10.3389/fendo.2022.982145 · Cited by 72 · see citing works
Control of mitochondrial function and cell growth by the atypical cadherin Fat1
Cao, L. L., Riascos‐Bernal, D. F., Chinnasamy, P., Dunaway, C. M., Hou, R., Pujato, M. A., O'Rourke, B. P., Miskolci, V., Guo, L., Hodgson, L., et al. (2016) · Nature · doi:10.1038/nature20170 · Cited by 67 · see citing works
Emerging role of mitochondria in airborne particulate matter-induced immunotoxicity
Sharma, J., Parsai, K., Raghuwanshi, P., Ali, S. A., Tiwari, V., Bhargava, A., & Mishra, P. K. (2020) · Environmental Pollution · doi:10.1016/j.envpol.2020.116242 · Cited by 66 · see citing works
Mechanisms of Atherosclerosis Induced by Postprandial Lipemia
Zhao, Y., Liu, L., Yang, S., Liu, G., Pan, L., Gu, C., Wang, Y., Li, D. X., Zhao, R., & Wu, M. (2021) · Frontiers in Cardiovascular Medicine · doi:10.3389/fcvm.2021.636947 · Cited by 62 · see citing works
Role of macrophage extracellular traps in innate immunity and inflammatory disease
Rasmussen, K. H., & Hawkins, C. L. (2022) · Biochemical Society Transactions · doi:10.1042/bst20210962 · Cited by 62 · see citing works
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Mitochondrial fidelity and metabolic agility control immune cell fate and function
Sack, M. N. (2018) · Journal of Clinical Investigation · doi:10.1172/jci120845 · Cited by 54 · see citing works
Mitochondrial regulation of macrophage cholesterol homeostasis
Graham, A. (2015) · Free Radical Biology and Medicine · doi:10.1016/j.freeradbiomed.2015.08.010 · Cited by 54 · see citing works
Senescence in Vascular Smooth Muscle Cells and Atherosclerosis
Zha, Y., Zhuang, W., Yang, Y., Zhou, Y., Li, H., & Liang, J. (2022) · Frontiers in Cardiovascular Medicine · doi:10.3389/fcvm.2022.910580 · Cited by 55 · see citing works
“Nevertheless, long-term mtDNA damage leads to mitochondrial dysfunction and more damaging ROS production, which induces cellular senescence and hastens atherosclerosis development (34).”
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The alterations of mitochondrial DNA in coronary heart disease
Hu, H., Lin, Y., Xu, X., Lin, S., Chen, X., & Wang, S. (2020) · Experimental and Molecular Pathology · doi:10.1016/j.yexmp.2020.104412 · Cited by 51 · see citing works
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Oxidative burden in familial hypercholesterolemia
Mollazadeh, H., Carbone, F., Montecucco, F., Pirro, M., & Sahebkar, A. (2018) · Journal of Cellular Physiology · doi:10.1002/jcp.26466 · Cited by 47 · see citing works
“Moreover, mtDNA damage induces VSMC apoptosis and accelerates all aspects of atherosclerosis in particular plaque rupture and mitochondrial outer membrane permeabilization (MPTP) opening and apoptosis (Emma & Bennett, 2014).”
BackgroundKoller, A., Fazzini, F., Lamina, C., Rantner, B., Kollerits, B., Stadler, M., Klein-Weigel, P. F., Fraedrich, G., & Kronenberg, F. (2020) · Journal of Internal Medicine · doi:10.1111/joim.13027 · Cited by 47 · see citing works
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Mechanotranduction Pathways in the Regulation of Mitochondrial Homeostasis in Cardiomyocytes
Liao, H., Qi, Y., Ye, Y., Yue, P., Zhang, D., & Li, Y. (2021) · Frontiers in Cell and Developmental Biology · doi:10.3389/fcell.2020.625089 · Cited by 44 · see citing works
“MtDNA damage further stimulates the production of ROS, forming a vicious cycle and aggravating the damage of CMs (Yu and Bennett, 2014; Lee et al., 2017).”
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Mitochondrial DNA: A Key Regulator of Anti-Microbial Innate Immunity
Kausar, S., Yang, L., Abbas, M. N., Hu, X., Zhao, Y., Zhu, Y., & Cui, H. (2020) · Genes · doi:10.3390/genes11010086 · Cited by 40 · see citing works
“Due to common ancestors, DNA of mitochondria shares characteristic features with the bacterial genome, as mitochondrial DNA also consists of unmethylated DNA as CpG islands [6].”
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“In atherosclerosis, oxidative damage and replication errors are the sources of mtDNA defects, which lead to mitochondrial dysfunction and directly promote atherosclerosis (Yu and Bennett, 2014).”
BackgroundAlvarado‐Vásquez, N. (2015) · Experimental Gerontology · doi:10.1016/j.exger.2015.05.010 · Cited by 39 · see citing works
“Recently, a review on the role of mtDNA in the development of atherosclerosiswas published (Yu and Bennett, 2014).”
BackgroundThe Role of Mitochondrial DNA in the Development of Ischemia Reperfusion Injury
Hu, Q., Zhou, Q., Wu, J., Wu, X., & Ren, J. (2018) · Shock · doi:10.1097/shk.0000000000001190 · Cited by 38 · see citing works
Markin, A. M., Sobenin, I. A., Grechko, A. V., Zhang, D., & Orekhov, A. N. (2020) · Frontiers in Pharmacology · doi:10.3389/fphar.2020.00642 · Cited by 39 · see citing works
Volobueva, A. S., Grechko, A. V., Yet, S., Sobenin, I. A., & Orekhov, A. N. (2019) · Biomolecules · doi:10.3390/biom9080377 · Cited by 38 · see citing works
“Mitochondrial dysfunction promotes lipolysis and the increase of serum free fatty acids and glycerol [10].”
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Immunostimulatory role of mitochondrial DAMPs: alarming for pre-eclampsia?
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Correlation between Mitochondrial Reactive Oxygen and Severity of Atherosclerosis
Dorighello, G. G., Paim, B. A., Kiihl, S. F., Ferreira, M. S., Catharino, R. R., Vercesi, A. E., & Oliveira, H. C. F. (2015) · Oxidative Medicine and Cellular Longevity · doi:10.1155/2016/7843685 · Cited by 31 · see citing works
“It has been well recognized that mitochondrial dysfunctions such as opening of the permeability transition pore directly promote inflammation and oxidative stress, phenomena involved in several cardiometabolic diseases [8, 9, 12].”
BackgroundLien, L., Chiou, H., Yeh, H., Chiu, S., Jeng, J., Lin, H., Hu, C., Hsieh, F., & Wei, Y. (2017) · Journal of the American Heart Association · doi:10.1161/jaha.117.006157 · Cited by 31 · see citing works
“Decreased mtDNA content was reported to result in excess mitochondrial ROS production.(33) Increased production of ROS, in turn, leads to oxidative damage to lipids, proteins, and mtDNA.”
BackgroundContis, A., Mitrovic, S., Lavie, J., Douchet, I., Lazaro, E., Truchetet, M., Goizet, C., Contin‐Bordes, C., Schaeverbeke, T., Blanco, P., et al. (2017) · Rheumatology · doi:10.1093/rheumatology/kex041 · Cited by 30 · see citing works
Liu, Y., Peng, C., & Wu, A. (2020) · Aging · doi:10.18632/aging.103120 · Cited by 30 · see citing works
“suggested that mitochondria [7], endothelial dysfunction [8], and interplay between inflammation and immune cells [9, 10] are associated with AS progression.”
BackgroundMitochondrial [dys]function; culprit in pre-eclampsia?
McCarthy, C., & Kenny, L. C. (2016) · Clinical Science · doi:10.1042/cs20160103 · Cited by 29 · see citing works
Cardiovascular Disease, Mitochondria, and Traditional Chinese Medicine
Wang, J., Lin, F., Guo, L., Xiong, X., & Fan, X. (2015) · Evidence-based Complementary and Alternative Medicine · doi:10.1155/2015/143145 · Cited by 28 · see citing works
“Mitochondria have been recognised as critical regulators of cell death, generation of ATP, and the generation of reactive oxygen species (ROS), and mtDNA damage leads to mitochondrial dysfunction and promotes atherosclerosis directly [43].”
BackgroundHernández‐Mijares, A., Bañuls, C., Rovira‐Llopis, S., Díaz‐Morales, N., Escribano‐López, I., de Pablo, C., Álvarez, Á., Veses, S., Rocha, M., & Víctor, V. M. (2016) · Atherosclerosis · doi:10.1016/j.atherosclerosis.2016.01.044 · Cited by 28 · see citing works
“Oxidative stress, mitochondrial dysfunction and inflammation are related to cardiovascular diseases (CVD) and atherogenesis [1].”
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Mitochondria-Derived Damage-Associated Molecular Patterns in Sepsis: From Bench to Bedside
Li, S., Hu, Q., Huang, J., Wu, X., & Ren, J. (2019) · Oxidative Medicine and Cellular Longevity · doi:10.1155/2019/6914849 · Cited by 28 · see citing works
“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].”
BackgroundErythrocytes: Member of the immune system that should not be ignored
Ren, Y., Yan, C., & Yang, H. (2023) · Critical Reviews in Oncology/Hematology · doi:10.1016/j.critrevonc.2023.104039 · Cited by 28 · see citing works
Heteroplasmic Variants of Mitochondrial DNA in Atherosclerotic Lesions of Human Aortic Intima
Sobenin, I. A., Zhelankin, A. V., Khasanova, Z. B., Sinyov, V. V., Medvedeva, L. V., Sagaidak, M. O., Makeev, V. J., Kolmychkova, K. I., Smirnova, A. S., Sukhorukov, V. N., et al. (2019) · Biomolecules · doi:10.3390/biom9090455 · Cited by 29 · see citing works
“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.”
BackgroundZhang, L., Zheng, X., Huang, Y., Ge, Y., Sun, M., Chen, W., Liu, W., & Li, X. (2021) · Comparative Biochemistry and Physiology Part C Toxicology & Pharmacology · doi:10.1016/j.cbpc.2021.109003 · Cited by 26 · see citing works
Li, Y., Yang, S., Jin, X., Li, D. X., Lu, J., Wang, X., & Wu, M. (2023) · Frontiers in Pharmacology · doi:10.3389/fphar.2023.1082817 · Cited by 26 · see citing works
“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…”
BackgroundAdvances in the study of the molecular biological mechanisms of radiation-induced brain injury.
Chen, G., Li, W. J., Xu, J., Pang, L., Tang, L., Yu, S., Li, A., Ge, H., Huang, R., & Cheng, H. (2023) · PubMed Central · Cited by 23 · see citing works
Dietary modulation of mitochondrial DNA damage: implications in aging and associated diseases
Lam, J., & McKeague, M. (2018) · The Journal of Nutritional Biochemistry · doi:10.1016/j.jnutbio.2018.07.003 · Cited by 23 · see citing works
Trimetazidine Protects Against Atherosclerosis by Changing Energy Charge and Oxidative Stress
Zheng, S., Du, Y., Peng, Q., Fan, X., Li, J., & Chen, M. (2018) · Medical Science Monitor · doi:10.12659/msm.911317 · Cited by 23 · see citing works
“Recent studies suggested that the development of atherosclerosis is also accompanied by energy depletion [9,10].”
BackgroundSalerno, 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 22 · see citing works
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Next-generation sequencing profiling of mitochondrial genomes in gout
Tseng, C., Chen, C., Yen, J., Huang, H., Chang, J., Chang, S., & Liao, W. (2018) · Arthritis Research & Therapy · doi:10.1186/s13075-018-1637-5 · Cited by 21 · see citing works
“Indeed, past studies have revealed causal roles of mitochondrial DNA (mtDNA) mutations and mitochondrial dysfunction in diseases with altered metabolism and inflammatory responses, for example, atherosclerosis [2].”
BackgroundRigotti, M., Cerbaro, A. F., Silva, I. D. R., Agostini, F., Branco, C. S., Moura, S., & Salvador, M. M. (2020) · Journal of Food Biochemistry · doi:10.1111/jfbc.13147 · Cited by 21 · see citing works
Luan, Y., Luan, Y., Jiao, Y., Liu, H., Huang, Z., Feng, Q., Pei, J., Yang, Y., & Ren, K. (2023) · Aging and Disease · doi:10.14336/ad.2023.1130 · Cited by 20 · see citing works
THE ROLE OF MUTAGENESIS IN ATHEROSCLEROSIS
Kutikhin, A. G., Sinitsky, M. Y., & Ponasenko, A. V. (2017) · Complex Issues of Cardiovascular Diseases · doi:10.17802/2306-1278-2017-1-92-101 · Cited by 20 · see citing works
“Повреждения митохондриальной ДНК Помимо мутаций в ядерной ДНК одним из ранних звеньев патогенеза атеросклероза являются мутации митохондриальной ДНК (мтДНК) [53-56].”
The aetiology of cardiovascular disease: a role for mitochondrial DNA?
Venter, M., van der Westhuizen, F. H., & Elson, J. L. (2018) · Cardiovascular journal of South Africa/Cardiovascular journal of Southern Africa · doi:10.5830/cvja-2017-037 · Cited by 20 · see citing works
“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…”
BackgroundExtracellular DNA in blood products and its potential effects on transfusion
Li, Y., Yang, D., Yang, Q., Fu, C., & Huang, Y. (2020) · Bioscience Reports · doi:10.1042/bsr20192770 · Cited by 20 · see citing works
Organelle dynamics of endothelial mitochondria in diabetic angiopathy
Xiang, H., Song, R., Ouyang, J., Zhu, R., Shu, Z., Liu, Y., Wang, X., Zhang, D., Zhao, J., & Lu, H. (2021) · European Journal of Pharmacology · doi:10.1016/j.ejphar.2021.173865 · Cited by 21 · see citing works
Hua, J., Gao, Z., Zhong, S., Wei, B., Zhu, J., & Ying, R. (2021) · Biochemical and Biophysical Research Communications · doi:10.1016/j.bbrc.2021.08.023 · Cited by 20 · see citing works
New insights into macrophage subsets in atherosclerosis
Wang, Y., Wang, Q. A., & Xu, D. (2022) · Journal of Molecular Medicine · doi:10.1007/s00109-022-02224-0 · Cited by 19 · see citing works
“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].”
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Studies of the Formation and Stability of Ezetimibe-Cyclodextrin Inclusion Complexes
Biernacka, M., Ilyich, T. V., Zavodnik, I. B., Palecz, B., & Stępniak, A. (2021) · International Journal of Molecular Sciences · doi:10.3390/ijms23010455 · Cited by 18 · see citing works
“It is well known that oxidative stress, mitochondrial dysfunction, and inflammation are related to cardiovascular diseases and atherogenesis [40].”
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Genetics of Arterial-Wall-Specific Mechanisms in Atherosclerosis: Focus on Mitochondrial Mutations
Orekhov, A. N., Ivanova, E. A., Markin, A. M., Nikiforov, N. G., & Sobenin, I. A. (2020) · Current Atherosclerosis Reports · doi:10.1007/s11883-020-00873-5 · Cited by 18 · see citing works
Mitochondrial DNA in Exercise-Mediated Innate Immune Responses
Wen, X., Fan, J., Duan, X., Zhu, X., Bai, J., & Zhang, T. (2025) · International Journal of Molecular Sciences · doi:10.3390/ijms26073069 · Cited by 17 · see citing works
“…activates the myeloid differentiation primary response gene 88 (MyD88), inducing the translocation of nuclear factor kappa-B NF-κ B) and interferon regulatory factor 7 (IRF7) into nucleus to enhance the expression of pro-inflammatory cytokines and type I interferon (IFN-I) respectively [15,36–38].”
Metabolic Strategies in Healthcare: A New Era
Phillips, M. C. L. (2022) · Aging and Disease · doi:10.14336/ad.2021.1018 · Cited by 16 · see citing works
“First, it does not sufficiently address the striking oxidative damage and mitochondria dysfunction observed in human plaques [13,14].”
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The role of hepatocyte mitochondrial DNA in liver injury
Xu, Y., Chu, C., Shi, Z., & Zhang, J. (2023) · Biomedicine & Pharmacotherapy · doi:10.1016/j.biopha.2023.115692 · Cited by 18 · see citing works
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Xu, J., Yang, H., Yang, L., Wang, Z., Qin, X., Zhou, J., Dong, L., Li, J., Zhu, M., Zhang, X., et al. (2021) · Cell Death and Disease · doi:10.1038/s41419-021-03462-9 · Cited by 12 · see citing works
Tian, F., Li, J., Liu, X., Tong, T., & Zhang, Z. (2015) · Archives of Gerontology and Geriatrics · doi:10.1016/j.archger.2015.11.004 · Cited by 12 · see citing works
Islam, M. N., Mishra, V. K., Munalisa, R., Parveen, F., Ali, S. F., Akter, K., Ahmed, T., Ho, T., & Huang, C. (2024) · Molecular & Cellular Toxicology · doi:10.1007/s13273-023-00424-4 · Cited by 11 · see citing works
“Atherosclerosis recently resulted in mitochondrial dysfunction and in particular mitochondrial DNA damage despite the poor contribution of mitochondrial to cardiac bioenergetics (Yu and Bennett 2014).”
Gasparini, P. V. F., Matias, A. M., Sales, S. T., Sarter, J. B. B., Siqueira, J. S., Corrêa, C. R., Lima‐Leopoldo, A. P., & Leopoldo, A. S. (2021) · Cellular Physiology and Biochemistry · doi:10.33594/000000441 · Cited by 11 · see citing works
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“Second, it is close to the electron transport chain, which is the main source of ROS production [35].”
BackgroundRoles of Mitochondrial DNA Signaling in Immune Responses
Wang, L., Liebmen, M., & Wang, X. (2017) · Advances in experimental medicine and biology · doi:10.1007/978-981-10-6674-0_4 · Cited by 9 · see citing works
Mitochondrial Respiration and Atherosclerosis
Forrester, S. J., & Griendling, K. K. (2017) · Arteriosclerosis Thrombosis and Vascular Biology · doi:10.1161/atvbaha.117.310298 · Cited by 9 · see citing works
Mitochondrial DNA in atherosclerosis research progress: a mini review
Liu, Z., Huang, N., Liu, C., Wu, C., Zhou, L., Liu, X., & Lei, H. (2025) · Frontiers in Immunology · doi:10.3389/fimmu.2025.1526390 · Cited by 7 · see citing works
“The complex interplay between mtDNA mutations, copy number abnormalities, release, and in fl ammation is increasingly recognized as a central driving factor in AS (13, 16, 17).”
Lin, Y., Yang, Q., Wang, J., Chen, X., Liu, Y., & Zhou, T. (2022) · Frontiers in Endocrinology · doi:10.3389/fendo.2022.962635 · Cited by 7 · see citing works
“Mitochondria have been recognized as key regulators of inflammation, cell death, metabolism and ROS production (61).”
Background
- 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
- 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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