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Artículos de revistas sobre el tema "Mitoepigenetics"

Autor: Grafiati
Publicado: 14 de marzo de 2023
Última modificación: 17 de junio 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 communicating to each other to regulate different cellular pathways. However, little is known about the mechanisms underlying mitoepigenetics and nuclei–mitochondria communication, and also about the involvement of the ncRNAs in mitochondrial functions and related diseases. In this context, this review presents the state-of-the-art knowledge, focusing on ncRNAs as new players in mitoepigenetic regulation and discussing future perspectives of these fields.
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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 levels. Fourth and most recent line of evidence indicates that mitochondrial DNA similar to ncDNA also is subject to epigenetic modifications, particularly by the 5-methylcytosine and 5-hydroxymethylcytosine marks. The latter interaction of mitochondria with epigenetics has been termed ‘mitochondrial epigenetics’. Here we summarize recent developments in this particular area of epigenetic research. Furthermore, we propose the term ‘mitoepigenetics’ to include all four above-noted types of interactions between mitochondria and epigenetics, and we suggest a more restricted usage of the term ‘mitochondrial epigenetics’ for molecular events dealing solely with the intra-mitochondrial epigenetics and the modifications of mitochondrial genome.
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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 the possibility of applying these advances for future AD therapy. Extensive research has suggested an important role of DNA methylation and hydroxymethylation, histone posttranslational modifications, and non-coding RNA regulation (with the emphasis on microRNAs) in the course and development of AD. Recent studies also indicated mitochondrial DNA (mtDNA) as an interesting biomarker of AD, since dysfunctions in the mitochondria and lower mtDNA copy number have been associated with AD pathophysiology. The current evidence suggests that epigenetic changes can be successfully detected, not only in the central nervous system, but also in the cerebrospinal fluid and on the periphery, contributing further to their potential as both biomarkers and therapeutic targets in AD.
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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 effect on male fetuses, although mitochondrial transcripts increased more so in females. Increased expression for several respiratory chain and adenosine triphosphate (ATP) synthase proteins were observed. However, fetal LV mitochondrial complex I and complex II/III activities were significantly decreased, likely contributing to a 73% decreased LV ATP content and increased LV lipid peroxidation. Moreover, MNR fetal LV mitochondria showed sparse and disarranged cristae. This study indicates that mitochondria are targets of the remodeling and imprinting processes in a sex-dependent manner. Mitochondrial ROS production and inadequate energy production add another layer of complexity. Altogether these observations raise the possibility that dysfunctional mitochondria in the fetus may contribute in turn to epigenetic memory of in utero stress in the adult. The role of mitoepigenetics and involvement of mitochondrial and genomic non-coding RNAs in mitochondrial functions and nuclei–mitochondria crosstalk with in utero stress awaits further investigation.
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10

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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11

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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12

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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13

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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14

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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15

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 led us to ask if mtDNA methylation has a role in maintaining mitochondrial genome stability. Herein, we report that mitochondrial genome undergoes de novo mtDNA methylation that can protect mtDNA against enhanced oxidative damage during the peri-implantation window. Mitochondrial genome gains extensive mtDNA methylation during transition from blastocysts to postimplantation embryos, thus establishing relatively hypermethylated mtDNA from hypomethylated state in blastocysts. Mechanistic study revealed that DNA methyltransferase 3A (DNMT3A) and DNMT3B enter mitochondria during this process and bind to mtDNA, via their unique mitochondrial targeting sequences. Importantly, loss- and gain-of-function analyses indicated that DNMT3A and DNMT3B are responsible for catalyzing de novo mtDNA methylation, in a synergistic manner. Finally, we proved, in vivo and in vitro, that increased mtDNA methylation functions to protect mitochondrial genome against mtDNA damage induced by increased mitochondrial oxidative stress. Together, we reveal mtDNA methylation dynamics and its underlying mechanism during the critical developmental window. We also provide the functional link between mitochondrial epigenetic remodeling and metabolic changes, which reveals a role for nuclear-mitochondrial crosstalk in establishing mitoepigenetics and maintaining mitochondrial homeostasis.
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16

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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