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Journal articles on the topic 'Epigenetic reprogramming'

Author: Grafiati

Published: 4 June 2021

Last updated: 26 July 2025

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1

Stoker, A. "Epigenetic reprogramming." Trends in Genetics 14, no. 2 (1998): 53. http://dx.doi.org/10.1016/s0168-9525(98)01410-3.

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2

de Lima Camillo, Lucas Paulo, and Robert B. A. Quinlan. "A ride through the epigenetic landscape: aging reversal by reprogramming." GeroScience 43, no. 2 (2021): 463–85. http://dx.doi.org/10.1007/s11357-021-00358-6.

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AbstractAging has become one of the fastest-growing research topics in biology. However, exactly how the aging process occurs remains unknown. Epigenetics plays a significant role, and several epigenetic interventions can modulate lifespan. This review will explore the interplay between epigenetics and aging, and how epigenetic reprogramming can be harnessed for age reversal. In vivo partial reprogramming holds great promise as a possible therapy, but several limitations remain. Rejuvenation by reprogramming is a young but rapidly expanding subfield in the biology of aging.

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Tada, Takashi, Hironobu Kimura, and Masako Tada. ""Nuclear Reprogramming" and "Epigenetic Reprogramming"." Journal of Mammalian Ova Research 21, no. 3 (2004): 97–104. http://dx.doi.org/10.1274/jmor.21.97.

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Watanabe, Akira, Yasuhiro Yamada, and Shinya Yamanaka. "Epigenetic regulation in pluripotent stem cells: a key to breaking the epigenetic barrier." Philosophical Transactions of the Royal Society B: Biological Sciences 368, no. 1609 (2013): 20120292. http://dx.doi.org/10.1098/rstb.2012.0292.

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The differentiation and reprogramming of cells are accompanied by drastic changes in the epigenetic profiles of cells. Waddington's classical model clearly describes how differentiating cells acquire their cell identity as the developmental potential of an individual cell population declines towards the terminally differentiated state. The recent discovery of induced pluripotent stem cells as well as of somatic cell nuclear transfer provided evidence that the process of differentiation can be reversed. The identity of somatic cells is strictly protected by an epigenetic barrier, and these cell

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5

Barneda-Zahonero, Bruna, Lidia Roman-Gonzalez, Olga Collazo, Tokameh Mahmoudi, and Maribel Parra. "Epigenetic Regulation of B Lymphocyte Differentiation, Transdifferentiation, and Reprogramming." Comparative and Functional Genomics 2012 (2012): 1–10. http://dx.doi.org/10.1155/2012/564381.

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B cell development is a multistep process that is tightly regulated at the transcriptional level. In recent years, investigators have shed light on the transcription factor networks involved in all the differentiation steps comprising B lymphopoiesis. The interplay between transcription factors and the epigenetic machinery involved in establishing the correct genomic landscape characteristic of each cellular state is beginning to be dissected. The participation of “epigenetic regulator-transcription factor” complexes is also crucial for directing cells during reprogramming into pluripotency or

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Li, Anqi, Rui Wang, Yuqiang Zhao, Peiran Zhao, and Jing Yang. "Crosstalk between Epigenetics and Metabolic Reprogramming in Metabolic Dysfunction-Associated Steatotic Liver Disease-Induced Hepatocellular Carcinoma: A New Sight." Metabolites 14, no. 6 (2024): 325. http://dx.doi.org/10.3390/metabo14060325.

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Epigenetic and metabolic reprogramming alterations are two important features of tumors, and their reversible, spatial, and temporal regulation is a distinctive hallmark of carcinogenesis. Epigenetics, which focuses on gene regulatory mechanisms beyond the DNA sequence, is a new entry point for tumor therapy. Moreover, metabolic reprogramming drives hepatocellular carcinoma (HCC) initiation and progression, highlighting the significance of metabolism in this disease. Exploring the inter-regulatory relationship between tumor metabolic reprogramming and epigenetic modification has become one of

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7

Giuliani, Stefano, Celeste Accetta, Simona di Martino, et al. "Metabolic Reprogramming in Melanoma: An Epigenetic Point of View." Pharmaceuticals 18, no. 6 (2025): 853. https://doi.org/10.3390/ph18060853.

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Metabolic reprogramming and epigenetic alterations are fundamental hallmarks of cancer cells, contributing to adaptation, progression, and resistance. In melanoma, high metabolic-epigenetic plasticity enables the rapid modulation of cell states in response to environmental and therapeutic pressures. Recent studies have highlighted a bidirectional crosstalk between cellular metabolism and epigenetic regulation. Epigenetic modifications influence the transcriptional control of metabolic genes, thereby shaping metabolic phenotypes. Conversely, specific metabolites are essential cofactors or subst

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8

Bunsick, David A., Jenna Matsukubo, and Myron R. Szewczuk. "Cannabinoids Transmogrify Cancer Metabolic Phenotype via Epigenetic Reprogramming and a Novel CBD Biased G Protein-Coupled Receptor Signaling Platform." Cancers 15, no. 4 (2023): 1030. http://dx.doi.org/10.3390/cancers15041030.

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The concept of epigenetic reprogramming predicts long-term functional health effects. This reprogramming can be activated by exogenous or endogenous insults, leading to altered healthy and different disease states. The exogenous or endogenous changes that involve developing a roadmap of epigenetic networking, such as drug components on epigenetic imprinting and restoring epigenome patterns laid down during embryonic development, are paramount to establishing youthful cell type and health. This epigenetic landscape is considered one of the hallmarks of cancer. The initiation and progression of

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9

Meiliana, Anna, and Andi Wijaya. "Epigenetic Reprogramming Induced Pluripotency." Indonesian Biomedical Journal 3, no. 2 (2011): 93. http://dx.doi.org/10.18585/inabj.v3i2.139.

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BACKGROUND: The ability to reprogram mature cells to an embryonic-like state by nuclear transfer or by inducing the expression of key transcription factors has provided us with critical opportunities to linearly map the epigenetic parameters that are essential for attaining pluripotency.CONTENT: Epigenetic reprogramming describes a switch in gene expression of one kind of cell to that of another unrelated cell type. Early studies in frog cloning provided some of the first experimental evidence for reprogramming. Subsequent procedures included mammalian somatic cell nuclear transfer, cell fusio

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10

Hörmanseder, Eva. "Epigenetic memory in reprogramming." Current Opinion in Genetics & Development 70 (October 2021): 24–31. http://dx.doi.org/10.1016/j.gde.2021.04.007.

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11

Suva, M. L., N. Riggi, and B. E. Bernstein. "Epigenetic Reprogramming in Cancer." Science 339, no. 6127 (2013): 1567–70. http://dx.doi.org/10.1126/science.1230184.

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12

Morgan, Hugh D., Fátima Santos, Kelly Green, Wendy Dean, and Wolf Reik. "Epigenetic reprogramming in mammals." Human Molecular Genetics 14, suppl_1 (2005): R47—R58. http://dx.doi.org/10.1093/hmg/ddi114.

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13

Consalvi, Silvia, Martina Sandoná, and Valentina Saccone. "Epigenetic Reprogramming of Muscle Progenitors: Inspiration for Clinical Therapies." Stem Cells International 2016 (2016): 1–11. http://dx.doi.org/10.1155/2016/6093601.

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In the context of regenerative medicine, based on the potential of stem cells to restore diseased tissues, epigenetics is becoming a pivotal area of interest. Therapeutic interventions that promote tissue and organ regeneration have as primary objective the selective control of gene expression in adult stem cells. This requires a deep understanding of the epigenetic mechanisms controlling transcriptional programs in tissue progenitors. This review attempts to elucidate the principle epigenetic regulations responsible of stem cells differentiation. In particular we focus on the current understa

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14

Buckberry, Sam, Xiaodong Liu, Daniel Poppe, et al. "Transient naive reprogramming corrects hiPS cells functionally and epigenetically." Nature 620, no. 7975 (2023): 863–72. http://dx.doi.org/10.1038/s41586-023-06424-7.

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AbstractCells undergo a major epigenome reconfiguration when reprogrammed to human induced pluripotent stem cells (hiPS cells). However, the epigenomes of hiPS cells and human embryonic stem (hES) cells differ significantly, which affects hiPS cell function1–8. These differences include epigenetic memory and aberrations that emerge during reprogramming, for which the mechanisms remain unknown. Here we characterized the persistence and emergence of these epigenetic differences by performing genome-wide DNA methylation profiling throughout primed and naive reprogramming of human somatic cells to

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15

Gomes, Kátia Maria Sampaio, Ismael Cabral Costa, Jeniffer Farias dos Santos, Paulo Magno Martins Dourado, Maria Fernanda Forni, and Julio Cesar Batista Ferreira. "Induced pluripotent stem cells reprogramming: Epigenetics and applications in the regenerative medicine." Revista da Associação Médica Brasileira 63, no. 2 (2017): 180–89. http://dx.doi.org/10.1590/1806-9282.63.02.180.

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Summary Induced pluripotent stem cells (iPSCs) are somatic cells reprogrammed into an embryonic-like pluripotent state by the expression of specific transcription factors. iPSC technology is expected to revolutionize regenerative medicine in the near future. Despite the fact that these cells have the capacity to self-renew, they present low efficiency of reprogramming. Recent studies have demonstrated that the previous somatic epigenetic signature is a limiting factor in iPSC performance. Indeed, the process of effective reprogramming involves a complete remodeling of the existing somatic epig

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16

Lombardo, Claudio. "Epigenetic Reprogramming: Evolutionary Synergies for the Prevention of Emerging Diseases." International Journal of Psychiatry 10, no. 01 (2025): 01–11. https://doi.org/10.33140/ijp.10.01.08.

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From the perspective of systems theory, human health results from a dynamic balance between environmental, biological, and behavioral factors [1]. The interaction between endocrine-disrupting chemicals (EDCs), sedentary lifestyles, ultraprocessed food consumption, and disconnection from natural stimuli disrupts circadian rhythms, metabolism, and brain functions, generating a state of neuroendocrine dysregulation and systemic inflammation [1,2]. Exposure to EDCs compromises hormonal and neurochemical regulation, with transgenerational effects that increase the risk of psychiatric and metabolic

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17

Fu, Yuanji, Raquel Francés, Claudia Monge, et al. "Metabolic and Epigenetic Mechanisms in Hepatoblastoma: Insights into Tumor Biology and Therapeutic Targets." Genes 15, no. 11 (2024): 1358. http://dx.doi.org/10.3390/genes15111358.

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Background: Hepatoblastoma, the most common pediatric liver malignancy, is characterized by significant molecular heterogeneity and poor prognosis in advanced stages. Recent studies highlight the importance of metabolic reprogramming and epigenetic dysregulation in hepatoblastoma pathogenesis. This review aims to explore the metabolic alterations and epigenetic mechanisms involved in hepatoblastoma and how these processes contribute to tumor progression and survival. Methods: Relevant literature on metabolic reprogramming, including enhanced glycolysis, mitochondrial dysfunction, and shifts in

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18

Christopeit, Maximilian. "Epigenetic reprogramming and blood development." Epigenomics 7, no. 1 (2015): 9–11. http://dx.doi.org/10.2217/epi.14.68.

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19

Pei, Yonggang, Josiah Hiu-yuen Wong, and Erle S. Robertson. "Herpesvirus Epigenetic Reprogramming and Oncogenesis." Annual Review of Virology 7, no. 1 (2020): 309–31. http://dx.doi.org/10.1146/annurev-virology-020420-014025.

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Among all of the known biological carcinogens, Epstein-Barr virus (EBV) and Kaposi's sarcoma-associated herpesvirus (KSHV) are two of the classical oncogenic herpesviruses known to induce the oncogenic phenotype. Many studies have revealed important functions related to epigenetic alterations of the EBV and KSHV genomes that mediate oncogenesis, but the detailed mechanisms are not fully understood. It is also challenging to fully describe the critical cellular events that drive oncogenesis as well as a comprehensive map of the molecular contributors. This review introduces the roles of epigene

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20

Hochedlinger, Konrad, and Rudolf Jaenisch. "Induced Pluripotency and Epigenetic Reprogramming." Cold Spring Harbor Perspectives in Biology 7, no. 12 (2015): a019448. http://dx.doi.org/10.1101/cshperspect.a019448.

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21

Hsu, Fei-Man, and Pao-Yang Chen. "Game theory in epigenetic reprogramming." Physics of Life Reviews 20 (March 2017): 143–45. http://dx.doi.org/10.1016/j.plrev.2017.01.005.

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22

Wasson, J. A., C. C. Ruppersburg, and D. J. Katz. "Restoring totipotency through epigenetic reprogramming." Briefings in Functional Genomics 12, no. 2 (2012): 118–28. http://dx.doi.org/10.1093/bfgp/els042.

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23

Hochedlinger, Konrad. "Transcription factor-induced epigenetic reprogramming." Cell Research 18, S1 (2008): S4. http://dx.doi.org/10.1038/cr.2008.94.

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24

Nam-Hyung Kim, Xiang-Shun Cui, and Yong Man Han. "Epigenetic reprogramming in cloned embryos." IEEE Engineering in Medicine and Biology Magazine 23, no. 2 (2004): 47–51. http://dx.doi.org/10.1109/memb.2004.1310974.

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25

Katsuyama, Tomonori, and Renato Paro. "Epigenetic reprogramming during tissue regeneration." FEBS Letters 585, no. 11 (2011): 1617–24. http://dx.doi.org/10.1016/j.febslet.2011.05.010.

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26

Cezar, Gabriela Gebrin. "Epigenetic Reprogramming of Cloned Animals." Cloning and Stem Cells 5, no. 3 (2003): 165–80. http://dx.doi.org/10.1089/153623003769645839.

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27

Hochedlinger, K., and K. Plath. "Epigenetic reprogramming and induced pluripotency." Development 136, no. 4 (2009): 509–23. http://dx.doi.org/10.1242/dev.020867.

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28

Lucifero, Diana, and Wolf Reik. "Artificial sperm and epigenetic reprogramming." Nature Biotechnology 24, no. 9 (2006): 1097–98. http://dx.doi.org/10.1038/nbt0906-1097.

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29

Ferrari, R., M. Pellegrini, G. A. Horwitz, W. Xie, A. J. Berk, and S. K. Kurdistani. "Epigenetic Reprogramming by Adenovirus e1a." Science 321, no. 5892 (2008): 1086–88. http://dx.doi.org/10.1126/science.1155546.

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30

Reik, W. "Epigenetic Reprogramming in Mammalian Development." Science 293, no. 5532 (2001): 1089–93. http://dx.doi.org/10.1126/science.1063443.

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31

Sindhu, Camille, Payman Samavarchi-Tehrani, and Alexander Meissner. "Transcription Factor-mediated Epigenetic Reprogramming." Journal of Biological Chemistry 287, no. 37 (2012): 30922–31. http://dx.doi.org/10.1074/jbc.r111.319046.

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32

Singh, Prim B., and Fred Zacouto. "Nuclear reprogramming and epigenetic rejuvenation." Journal of Biosciences 35, no. 2 (2010): 315–19. http://dx.doi.org/10.1007/s12038-010-0034-2.

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33

Li, Wei, and Qi Zhou. "Epigenetic reprogramming: roads to pluripotency." Frontiers in Biology 5, no. 1 (2009): 8–11. http://dx.doi.org/10.1007/s11515-010-0003-z.

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34

Chen, Jiekai, and Duanqing Pei. "Epigenetic Landmarks During Somatic Reprogramming." IUBMB Life 68, no. 11 (2016): 854–57. http://dx.doi.org/10.1002/iub.1577.

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35

Meiliana, Anna, Nurrani Mustika Dewi, and Andi Wijaya. "Metabolic Reprogramming and Molecular Rewiring in Cancer: Therapeutic Opportunities." Indonesian Biomedical Journal 13, no. 2 (2021): 114–39. http://dx.doi.org/10.18585/inabj.v13i2.1598.

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BACKGROUND: A lot of contemporary cancer research has concentrated on genetic influence. However, cancer also involves biochemical changes, such as metabolic adaptation to support the aberrant cell proliferation.CONTENT: The fast cell proliferation in cancer cells enforce a metabolic re-arrangement to promote their long-term survival. The increased glucose uptake and fermentation of glucose to lactate are common features of this altered metabolism known as “the Warburg effect”. These metabolic pathways regulation enable cancer cells to produce adenosine triphosphate (ATP) in an efficient way.

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36

Bassal, Mahmoud Adel. "The Interplay between Dysregulated Metabolism and Epigenetics in Cancer." Biomolecules 13, no. 6 (2023): 944. http://dx.doi.org/10.3390/biom13060944.

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Cellular metabolism (or energetics) and epigenetics are tightly coupled cellular processes. It is arguable that of all the described cancer hallmarks, dysregulated cellular energetics and epigenetics are the most tightly coregulated. Cellular metabolic states regulate and drive epigenetic changes while also being capable of influencing, if not driving, epigenetic reprogramming. Conversely, epigenetic changes can drive altered and compensatory metabolic states. Cancer cells meticulously modify and control each of these two linked cellular processes in order to maintain their tumorigenic potenti

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37

Youness, Eman. "Overview on Epigenetics and Cancer." Clinical Medical Reviews and Reports 2, no. 3 (2020): 01–06. http://dx.doi.org/10.31579/2690-8794/015.

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Epigenetics is considered as the science of hereditary phenotype which does not encompass amendment in the DNA. This occurs through chemical processes that modify the phenotype, without altering the genotype. A large number of studies showed that metabolic diseases are highly associated with epigenetic alterations suggesting that epigenetic factors may play a central role in cancer. Recent advancements in the rapidly evolving field of cancer epigenetics have shown extensive reprogramming of every component of the epigenetic machinery in cancer including DNA methylation, histone modifications,

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38

Wang, Guangchao, and Jingdong J. Han. "Connections between metabolism and epigenetic modifications in cancer." Medical Review 1, no. 2 (2021): 199–221. http://dx.doi.org/10.1515/mr-2021-0015.

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Abstract How cells sense and respond to environmental changes is still a key question. It has been identified that cellular metabolism is an important modifier of various epigenetic modifications, such as DNA methylation, histone methylation and acetylation and RNA N6-methyladenosine (m6A) methylation. This closely links the environmental nutrient availability to the maintenance of chromatin structure and gene expression, and is crucial to regulate cellular homeostasis, cell growth and differentiation. Cancer metabolic reprogramming and epigenetic alterations are widely observed, and facilitat

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39

Srivastava, Anusha, Ankit Srivastava, and Rajnish Kumar Singh. "Insight into the Epigenetics of Kaposi’s Sarcoma-Associated Herpesvirus." International Journal of Molecular Sciences 24, no. 19 (2023): 14955. http://dx.doi.org/10.3390/ijms241914955.

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Epigenetic reprogramming represents a series of essential events during many cellular processes including oncogenesis. The genome of Kaposi’s sarcoma-associated herpesvirus (KSHV), an oncogenic herpesvirus, is predetermined for a well-orchestrated epigenetic reprogramming once it enters into the host cell. The initial epigenetic reprogramming of the KSHV genome allows restricted expression of encoded genes and helps to hide from host immune recognition. Infection with KSHV is associated with Kaposi’s sarcoma, multicentric Castleman’s disease, KSHV inflammatory cytokine syndrome, and primary ef

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40

Jasper, Heinrich. "AGING REPROGRAMMED." Innovation in Aging 8, Supplement_1 (2024): 268. https://doi.org/10.1093/geroni/igae098.0867.

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Abstract Epigenetic reprogramming of differentiated cells into stem-like or plastic cells is a feature of regenerative processes in many tissues. This process can be leveraged to induce full pluripotency, which essentially represents a fully rejuvenated state of the epigenome. Evidence is now accumulating that partial in vivo epigenetic reprogramming, where reprogramming to pluripotency is initiated but not completed, can alleviate age-related dysfunction in tissue repair, and even extend lifespan. In a wide range of disease models, reprogramming has been shown to improve outcomes and promote

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41

Seisenberger, Stefanie, Julian R. Peat, Timothy A. Hore, Fátima Santos, Wendy Dean, and Wolf Reik. "Reprogramming DNA methylation in the mammalian life cycle: building and breaking epigenetic barriers." Philosophical Transactions of the Royal Society B: Biological Sciences 368, no. 1609 (2013): 20110330. http://dx.doi.org/10.1098/rstb.2011.0330.

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In mammalian development, epigenetic modifications, including DNA methylation patterns, play a crucial role in defining cell fate but also represent epigenetic barriers that restrict developmental potential. At two points in the life cycle, DNA methylation marks are reprogrammed on a global scale, concomitant with restoration of developmental potency. DNA methylation patterns are subsequently re-established with the commitment towards a distinct cell fate. This reprogramming of DNA methylation takes place firstly on fertilization in the zygote, and secondly in primordial germ cells (PGCs), whi

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42

Feinberg, Andrew P. "Epigenetics of Hematopoiesis, Stem Cell Reprogramming, and Cancer." Blood 122, no. 21 (2013): SCI—47—SCI—47. http://dx.doi.org/10.1182/blood.v122.21.sci-47.sci-47.

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Abstract Since the discovery of altered DNA methylation in cancer in 1982, most studies of cancer epigenetics have focused on epimutations which could serve as surrogates of mutation. In the past decade, we and our collaborators have been leading efforts to develop whole-genome approaches to epigenetic analysis of human disease, that include novel approaches to array-based analysis and whole-genome bisulfite sequencing. This has led to the first whole-genome bisulfite sequencing methylation map of the cancer genome. Surprising results have been the discovery of CpG island shores and large hypo

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43

De Felici, Massimo. "Nuclear Reprogramming in Mouse Primordial Germ Cells: Epigenetic Contribution." Stem Cells International 2011 (2011): 1–15. http://dx.doi.org/10.4061/2011/425863.

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The unique capability of germ cells to give rise to a new organism, allowing the transmission of primary genetic information from generation to generation, depends on their epigenetic reprogramming ability and underlying genomic totipotency. Recent studies have shown that genome-wide epigenetic modifications, referred to as “epigenetic reprogramming”, occur during the development of the gamete precursors termed primordial germ cells (PGCs) in the embryo. This reprogramming is likely to be critical for the germ line development itself and necessary to erase the parental imprinting and setting t

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44

Yusuf, Abdurrahman Pharmacy, Murtala Bello Abubakar, Ibrahim Malami, et al. "Zinc Metalloproteins in Epigenetics and Their Crosstalk." Life 11, no. 3 (2021): 186. http://dx.doi.org/10.3390/life11030186.

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More than half a century ago, zinc was established as an essential micronutrient for normal human physiology. In silico data suggest that about 10% of the human proteome potentially binds zinc. Many proteins with zinc-binding domains (ZBDs) are involved in epigenetic modifications such as DNA methylation and histone modifications, which regulate transcription in physiological and pathological conditions. Zinc metalloproteins in epigenetics are mainly zinc metalloenzymes and zinc finger proteins (ZFPs), which are classified into writers, erasers, readers, editors, and feeders. Altogether, these

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45

Maali, Amirhosein, Faezeh Maroufi, Farzin Sadeghi, et al. "Induced pluripotent stem cell technology: trends in molecular biology, from genetics to epigenetics." Epigenomics 13, no. 8 (2021): 631–47. http://dx.doi.org/10.2217/epi-2020-0409.

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Induced pluripotent stem cell (iPSC) technology, based on autologous cells’ reprogramming to the embryonic state, is a new approach in regenerative medicine. Current advances in iPSC technology have opened up new avenues for multiple applications, from basic research to clinical therapy. Thus, conducting iPSC trials have attracted increasing attention and requires an extensive understanding of the molecular basis of iPSCs. Since iPSC reprogramming is based on the methods inducing the expression of specific genes involved in pluripotency states, it can be concluded that iPSC reprogramming is st

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46

Zhou, Yang, Sahar Alimohamadi, Li Wang, et al. "A Loss of Function Screen of Epigenetic Modifiers and Splicing Factors during Early Stage of Cardiac Reprogramming." Stem Cells International 2018 (2018): 1–14. http://dx.doi.org/10.1155/2018/3814747.

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Direct reprogramming of cardiac fibroblasts (CFs) to induced cardiomyocytes (iCMs) is a newly emerged promising approach for cardiac regeneration, disease modeling, and drug discovery. However, its potential has been drastically limited due to the low reprogramming efficiency and largely unknown underlying molecular mechanisms. We have previously screened and identified epigenetic factors related to histone modification during iCM reprogramming. Here, we used shRNAs targeting an additional battery of epigenetic factors involved in chromatin remodeling and RNA splicing factors to further identi

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Fernández-Santiago, Rubén, and Mario Ezquerra. "Epigenetic Research of Neurodegenerative Disorders Using Patient iPSC-Based Models." Stem Cells International 2016 (2016): 1–16. http://dx.doi.org/10.1155/2016/9464591.

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Epigenetic mechanisms play a role in human disease but their involvement in pathologies from the central nervous system has been hampered by the complexity of the brain together with its unique cellular architecture and diversity. Until recently, disease targeted neural types were only available as postmortem materials after many years of disease evolution. Current in vitro systems of induced pluripotent stem cells (iPSCs) generated by cell reprogramming of somatic cells from patients have provided valuable disease models recapitulating key pathological molecular events. Yet whether cell repro

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48

Zhang, Xiaolei, Shaorong Gao, and Xiaoyu Liu. "Advance in the Role of Epigenetic Reprogramming in Somatic Cell Nuclear Transfer-Mediated Embryonic Development." Stem Cells International 2021 (February 4, 2021): 1–13. http://dx.doi.org/10.1155/2021/6681337.

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Somatic cell nuclear transfer (SCNT) enables terminally differentiated somatic cells to gain totipotency. Many species are successfully cloned up to date, including nonhuman primate. With this technology, not only the protection of endangered animals but also human therapeutics is going to be a reality. However, the low efficiency of the SCNT-mediated reprogramming and the defects of extraembryonic tissues as well as abnormalities of cloned individuals limit the application of reproductive cloning on animals. Also, due to the scarcity of human oocytes, low efficiency of blastocyst development

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49

Niimi, Peter, Morgan Levine, and and Margarita Meer. "Epigenetic Trajectories of Aging and Reprogramming." Innovation in Aging 5, Supplement_1 (2021): 664–65. http://dx.doi.org/10.1093/geroni/igab046.2508.

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Abstract The epigenetic landscape is remodeled with age, bringing about widespread consequences for cell function. With the revolutionary discoveries by Yamanaka and Takahashi, as well as those that built on this work, the transcription factors Oct4, Sox2, KLF4, and C-Myc (OSKM) can be expressed in a variety of cells, including fibroblasts, to make iPSCs. Once cells are reprogrammed, they show an erasure of epigenetic remodeling, suggesting an avenue to reverse aging. It has been recently shown that ectopic expression of three factors, OSK, can restore vision in mouse glaucoma model and reduce

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Monteiro, Fabio Morato, Clara Slade Oliveira, Letícia Zoccolaro Oliveira, et al. "Chromatin Modifying Agents in theIn VitroProduction of Bovine Embryos." Veterinary Medicine International 2011 (2011): 1–9. http://dx.doi.org/10.4061/2011/694817.

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The low efficiency observed in cloning by nuclear transfer is related to an aberrant gene expression following errors in epigenetic reprogramming. Recent studies have focused on further understanding of the modifications that take place in the chromatin of embryos during the preimplantation period, through the use of chromatin modifying agents. The goal of these studies is to identify the factors involved in nuclear reprogramming and to adjustin vitromanipulations in order to better mimicin vivoconditions. Therefore, proper knowledge of epigenetic reprogramming is necessary to prevent possible

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