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Artículos de revistas sobre el tema "Mitoepigenetics"

Autor: Grafiati
Publicado: 14 de marzo de 2023
Última modificación: 26 de julio de 2025

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1

Cavalcante, Giovanna C., Leandro Magalhães, Ândrea Ribeiro-dos-Santos, and Amanda F. Vidal. "Mitochondrial Epigenetics: Non-Coding RNAs as a Novel Layer of Complexity." International Journal of Molecular Sciences 21, no. 5 (2020): 1838. http://dx.doi.org/10.3390/ijms21051838.

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Mitochondria are organelles responsible for several functions involved in cellular balance, including energy generation and apoptosis. For decades now, it has been well-known that mitochondria have their own genetic material (mitochondrial DNA), which is different from nuclear DNA in many ways. More recently, studies indicated that, much like nuclear DNA, mitochondrial DNA is regulated by epigenetic factors, particularly DNA methylation and non-coding RNAs (ncRNAs). This field is now called mitoepigenetics. Additionally, it has also been established that nucleus and mitochondria are constantly
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2

Lozano-Rosas, María Guadalupe, Enrique Chávez, Alejandro Rusbel Aparicio-Cadena, Gabriela Velasco-Loyden, and Victoria Chagoya de Sánchez. "Mitoepigenetics and hepatocellular carcinoma." Hepatoma Research 4, no. 6 (2018): 19. http://dx.doi.org/10.20517/2394-5079.2018.48.

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3

Sadakierska-Chudy, Anna, Małgorzata Frankowska, and Małgorzata Filip. "Mitoepigenetics and drug addiction." Pharmacology & Therapeutics 144, no. 2 (2014): 226–33. http://dx.doi.org/10.1016/j.pharmthera.2014.06.002.

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4

Ghosh, Sourav, Keshav K. Singh, Shantanu Sengupta, and Vinod Scaria. "Mitoepigenetics: The different shades of grey." Mitochondrion 25 (November 2015): 60–66. http://dx.doi.org/10.1016/j.mito.2015.09.003.

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5

Cao, Ke, Zhihui Feng, Feng Gao, Weijin Zang, and Jiankang Liu. "Mitoepigenetics: An intriguing regulatory layer in aging and metabolic-related diseases." Free Radical Biology and Medicine 177 (December 2021): 337–46. http://dx.doi.org/10.1016/j.freeradbiomed.2021.10.031.

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6

Lima, Camila Bruna, and Marc‐André Sirard. "Mitoepigenetics: Methylation of mitochondrial DNA is strand‐biased in bovine oocytes and embryos." Reproduction in Domestic Animals 55, no. 10 (2020): 1455–58. http://dx.doi.org/10.1111/rda.13786.

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7

Manev, Hari, and Svetlana Dzitoyeva. "Progress in mitochondrial epigenetics." BioMolecular Concepts 4, no. 4 (2013): 381–89. http://dx.doi.org/10.1515/bmc-2013-0005.

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AbstractMitochondria, intracellular organelles with their own genome, have been shown capable of interacting with epigenetic mechanisms in at least four different ways. First, epigenetic mechanisms that regulate the expression of nuclear genome influence mitochondria by modulating the expression of nuclear-encoded mitochondrial genes. Second, a cell-specific mitochondrial DNA content (copy number) and mitochondrial activity determine the methylation pattern of nuclear genes. Third, mitochondrial DNA variants influence the nuclear gene expression patterns and the nuclear DNA (ncDNA) methylation
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8

Nikolac Perkovic, Matea, Alja Videtic Paska, Marcela Konjevod, et al. "Epigenetics of Alzheimer’s Disease." Biomolecules 11, no. 2 (2021): 195. http://dx.doi.org/10.3390/biom11020195.

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There are currently no validated biomarkers which can be used to accurately diagnose Alzheimer’s disease (AD) or to distinguish it from other dementia-causing neuropathologies. Moreover, to date, only symptomatic treatments exist for this progressive neurodegenerative disorder. In the search for new, more reliable biomarkers and potential therapeutic options, epigenetic modifications have emerged as important players in the pathogenesis of AD. The aim of the article was to provide a brief overview of the current knowledge regarding the role of epigenetics (including mitoepigenetics) in AD, and
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9

Booz, George W., Gaelle P. Massoud, Raffaele Altara, and Fouad A. Zouein. "Unravelling the impact of intrauterine growth restriction on heart development: insights into mitochondria and sexual dimorphism from a non-hominoid primate." Clinical Science 135, no. 14 (2021): 1767–72. http://dx.doi.org/10.1042/cs20210524.

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Abstract Fetal exposure to an unfavorable intrauterine environment programs an individual to have a greater susceptibility later in life to non-communicable diseases, such as coronary heart disease, but the molecular processes are poorly understood. An article in Clinical Science recently reported novel details on the effects of maternal nutrient reduction (MNR) on fetal heart development using a primate model that is about 94% genetically similar to humans and is also mostly monotocous. MNR adversely impacted fetal left ventricular (LV) mitochondria in a sex-dependent fashion with a greater e
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10

Salunke, Chaitali* Deokar Shivprasad Dr. Kawade Rajendra Pathade Pratiksha. "Epigenetic Modification in Alzheimer Disease." International Journal of Pharmaceutical Sciences 2, no. 11 (2024): 1357–65. https://doi.org/10.5281/zenodo.14222567.

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Alzheimer’s disease (AD) is a devastating neurodegenerative disorder characterized by progressive cognitive decline and memory loss, imposing a significant burden on affected individuals and their families. Despite the recent promising progress in therapeutic approaches, more needs to be done to understand the intricate molecular mechanisms underlying the development and progression of AD. Alzheimer’s disease is characterized by the formation and deposit abnormal peptides such as amyloid plaques and neurofibrillary tangles in the Brain. There are currently no validated biomarkers w
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11

Ferreira, André, Teresa L. Serafim, Vilma A. Sardão, and Teresa Cunha-Oliveira. "Role of mtDNA-related mitoepigenetic phenomena in cancer." European Journal of Clinical Investigation 45 (December 18, 2014): 44–49. http://dx.doi.org/10.1111/eci.12359.

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12

Mishra, Pradyumna Kumar, Arpit Bhargava, Roshani Kumari, et al. "Integrated mitoepigenetic signalling mechanisms associated with airborne particulate matter exposure: A cross-sectional pilot study." Atmospheric Pollution Research 13, no. 5 (2022): 101399. http://dx.doi.org/10.1016/j.apr.2022.101399.

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13

Coppedè, Fabio, and Andrea Stoccoro. "Mitoepigenetics and Neurodegenerative Diseases." Frontiers in Endocrinology 10 (February 19, 2019). http://dx.doi.org/10.3389/fendo.2019.00086.

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14

Bruna de Lima, Camila, Erika Cristina dos Santos, and Marc-Andre Sirard. "The interplay between early embryo metabolism and mitoepigenetic programming of development." Reproduction, May 2023. http://dx.doi.org/10.1530/rep-22-0424.

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Initially perceived simply as an ATP producer, mitochondria also participate in a wide range of other cellular functions. Mitochondrial communication with the nucleus, as well as signaling to other cellular compartments is critical to cell homeostasis. Therefore, during early mammalian development, mitochondrial function is reported as a key element for survival. Any mitochondrial dysfunction may reflect in poor oocyte quality and may impair embryo development with possible long-lasting consequences to cell functions and the overall embryo phenotype. Growing evidence suggests that the availabi
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15

Dong, Zhen, Longjun Pu, and Hongjuan Cui. "Mitoepigenetics and Its Emerging Roles in Cancer." Frontiers in Cell and Developmental Biology 8 (January 23, 2020). http://dx.doi.org/10.3389/fcell.2020.00004.

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16

Hatawsh, Abdulrahman, Roya Hadi Al-Haddad, Ukamaka Gladys Okafor, et al. "Mitoepigenetics pathways and natural compounds: a dual approach to combatting hepatocellular carcinoma." Medical Oncology 41, no. 12 (2024). http://dx.doi.org/10.1007/s12032-024-02538-8.

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17

Ceylan, Deniz, Hidayet Ece Arat-Çelik, and İzel Cemre Aksahin. "Integrating mitoepigenetics into research in mood disorders: a state-of-the-art review." Frontiers in Physiology 15 (February 8, 2024). http://dx.doi.org/10.3389/fphys.2024.1338544.

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Mood disorders, including major depressive disorder and bipolar disorder, are highly prevalent and stand among the leading causes of disability. Despite the largely elusive nature of the molecular mechanisms underpinning these disorders, two pivotal contributors—mitochondrial dysfunctions and epigenetic alterations—have emerged as significant players in their pathogenesis. This state-of-the-art review aims to present existing data on epigenetic alterations in the mitochondrial genome in mood disorders, laying the groundwork for future research into their pathogenesis. Associations between abno
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18

Chen, Kuo, Pengwei Lu, Narasimha M. Beeraka, et al. "Mitochondrial mutations and mitoepigenetics: Focus on regulation of oxidative stress-induced responses in breast cancers." Seminars in Cancer Biology, October 2020. http://dx.doi.org/10.1016/j.semcancer.2020.09.012.

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19

Donato, Luigi, Domenico Mordà, Concetta Scimone, Simona Alibrandi, Rosalia D'Angelo, and Antonina Sidoti. "From powerhouse to regulator: The role of mitoepigenetics in mitochondrion-related cellular functions and human diseases." Free Radical Biology and Medicine, March 2024. http://dx.doi.org/10.1016/j.freeradbiomed.2024.03.025.

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20

Grady, Clare I., Lisa M. Walsh, and John D. Heiss. "Mitoepigenetics and gliomas: epigenetic alterations to mitochondrial DNA and nuclear DNA alter mtDNA expression and contribute to glioma pathogenicity." Frontiers in Neurology 14 (May 30, 2023). http://dx.doi.org/10.3389/fneur.2023.1154753.

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Epigenetic mechanisms allow cells to fine-tune gene expression in response to environmental stimuli. For decades, it has been known that mitochondria have genetic material. Still, only recently have studies shown that epigenetic factors regulate mitochondrial DNA (mtDNA) gene expression. Mitochondria regulate cellular proliferation, apoptosis, and energy metabolism, all critical areas of dysfunction in gliomas. Methylation of mtDNA, alterations in mtDNA packaging via mitochondrial transcription factor A (TFAM), and regulation of mtDNA transcription via the micro-RNAs (mir 23-b) and long noncod
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21

Yue, Yuan, Likun Ren, Chao Zhang, et al. "Mitochondrial genome undergoes de novo DNA methylation that protects mtDNA against oxidative damage during the peri-implantation window." Proceedings of the National Academy of Sciences 119, no. 30 (2022). http://dx.doi.org/10.1073/pnas.2201168119.

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Mitochondrial remodeling during the peri-implantation stage is the hallmark event essential for normal embryogenesis. Among the changes, enhanced oxidative phosphorylation is critical for supporting high energy demands of postimplantation embryos, but increases mitochondrial oxidative stress, which in turn threatens mitochondrial DNA (mtDNA) stability. However, how mitochondria protect their own histone-lacking mtDNA, during this stage remains unclear. Concurrently, the mitochondrial genome gain DNA methylation by this stage. Its spatiotemporal coincidence with enhanced mitochondrial stress le
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22

Chen, Kuo, Pengwei Lu, Narasimha M. Beeraka, et al. "Corrigendum to “Mitochondrial mutations and mitoepigenetics: Focus on regulation of oxidative stress-induced responses in breast cancers” [Semin. Cancer Biol. 83 (2022) 556–569]." Seminars in Cancer Biology, July 2022. http://dx.doi.org/10.1016/j.semcancer.2022.07.002.

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23

Dragoni, Francesca, Jessica Garau, Simona Orcesi, et al. "Comparison between D-loop methylation and mtDNA copy number in patients with Aicardi-Goutières Syndrome." Frontiers in Endocrinology 14 (March 14, 2023). http://dx.doi.org/10.3389/fendo.2023.1152237.

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IntroductionAicardi-Goutières Syndrome (AGS) is a rare encephalopathy with early onset that can be transmitted in both dominant and recessive forms. Its phenotypic covers a wide range of neurological and extraneurological symptoms. Nine genes that are all involved in nucleic acids (NAs) metabolism or signaling have so far been linked to the AGS phenotype. Recently, a link between autoimmune or neurodegenerative conditions and mitochondrial dysfunctions has been found. As part of the intricate system of epigenetic control, the mtDNA goes through various alterations. The displacement (D-loop) re
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24

Neikirk, Kit, Suraj Thapliyal, Sepiso K. Masenga, et al. "Mitoepigenetic targeting of age-related dysfunction: mechanisms, therapeutic avenues, and transgenerational implications." Aging Advances, June 11, 2025. https://doi.org/10.4103/agingadv.agingadv-d-25-00006.

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Mitochondrial epigenetics, a burgeoning field bridging mitochondrial biology and epigenetic regulation, has emerged as a critical determinant of aging and age-related diseases. While nuclear epigenetics is well-characterized, the mechanisms governing mitochondrial DNA (mtDNA) regulation, including nucleoid dynamics, non-coding RNAs (ncRNAs), and metabolite-driven modifications, remain underexplored. This review synthesizes evidence that mitochondrial epigenetics influences cardiovascular pathogenesis through altered DNA methylation and histone acetylation patterns, which dysregulate oxidative
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25

Mongelli, Alessia, Alessandro Mengozzi, Martin Geiger, et al. "Mitochondrial epigenetics in aging and cardiovascular diseases." Frontiers in Cardiovascular Medicine 10 (July 13, 2023). http://dx.doi.org/10.3389/fcvm.2023.1204483.

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Mitochondria are cellular organelles which generate adenosine triphosphate (ATP) molecules for the maintenance of cellular energy through the oxidative phosphorylation. They also regulate a variety of cellular processes including apoptosis and metabolism. Of interest, the inner part of mitochondria—the mitochondrial matrix—contains a circular molecule of DNA (mtDNA) characterised by its own transcriptional machinery. As with genomic DNA, mtDNA may also undergo nucleotide mutations that have been shown to be responsible for mitochondrial dysfunction. During physiological aging, the mitochondria
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26

Zheng, Longbin, Xiang Chen, Xian He, et al. "METTL4-Mediated Mitochondrial DNA N6-Methyldeoxyadenosine Promoting Macrophage Inflammation and Atherosclerosis." Circulation, December 17, 2024. https://doi.org/10.1161/circulationaha.124.069574.

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BACKGROUND: Mitochondrial dysfunction is a key factor in the development of atherogenesis. METTL4 (methyltransferase-like protein 4) mediates N6- methyldeoxyadenosine (6mA) of mammalian mitochondrial DNA (mtDNA). However, the role of METTL4-mediated mitoepigenetic regulation in atherosclerosis is still unknown. This study aims to investigate the potential involvement of METTL4 in atherosclerosis, explore the underlying mechanism, and develop targeted strategies for treating atherosclerosis. METHODS: Expression levels of mtDNA 6mA and METTL4 were determined in atherosclerotic lesions. We explor
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