The myeloproliferative neoplasms (MPNs) are a group of acquired clonal disorders where mutations drive proliferative disease resulting in increased blood counts and in some cases end-stage myelofibrosis. Epigenetic changes are the reversible modifications to DNA- and RNA-associated proteins that impact gene activity without changing the DNA sequence. This review summarizes mechanisms of epigenetic changes and the nucleosome. The drivers and epigenetic regulators in MPNs are outlined. In MPNs, distinct patterns of epigenetic dysregulation have been seen in chronic and in advanced phases. Methylation age and histone modification are altered in MPNs and by further treatment. The alterations found in methylation age in MPNs and with treatment are discussed, and the changes in histone modification with Janus kinase (JAK) inhibition are evaluated. Currently available therapeutic areas where the epigenome can be altered are outlined. Thus, we review the current knowledge and understanding of epigenetics in MPN and consider further management options. Understanding the epigenome and its alteration in MPNs and epigenetic changes associated with the progression of disease will lead to advances in therapeutic options.
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http://dx.doi.org/10.3389/fonc.2023.1206965 | DOI Listing |
Mol Genet Genomics
January 2025
Department of Emergency, Xiangyang No. 1 People's Hospital, Hubei University of Medicine, Xiangyang, 441000, China.
Acute kidney injury (AKI) is one of the most serious and common complications in the course of sepsis, known for its poor prognosis and high mortality rate. Recently, ferroptosis, as a newly discovered regulatory cell death, might be closely associated with the progression of AKI. METTL14 is a writer of RNA m6A, an abundant epigenetic modification in transcriptome with broad function.
View Article and Find Full Text PDFFront Aging
January 2025
Cellular and Molecular Neurobiology & Drug Targeting Laboratory, Department of Zoology, Indira Gandhi National Tribal University, Amarkantak, Madhya Pradesh, India.
Memory formation is associated with constant modifications of neuronal networks and synaptic plasticity gene expression in response to different environmental stimuli and experiences. Dysregulation of synaptic plasticity gene expression affects memory during aging and neurodegenerative diseases. Covalent modifications such as methylation on DNA and acetylation on histones regulate the transcription of synaptic plasticity genes.
View Article and Find Full Text PDFFront Cell Dev Biol
January 2025
Department of Human Genetics, Leiden University Medical Center (LUMC), Leiden, Netherlands.
Muscle repair and regeneration are complex processes. In Duchenne muscular dystrophy (DMD), these processes are disrupted by the loss of functional dystrophin, a key part of the transmembrane dystrophin-associated glycoprotein complex that stabilizes myofibers, indirectly leading to progressive muscle wasting, subsequent loss of ambulation, respiratory and cardiac insufficiency, and premature death. As part of the DMD pathology, histone deacetylase (HDAC) activity is constitutively increased, leading to epigenetic changes and inhibition of muscle regeneration factors, chronic inflammation, fibrosis, and adipogenesis.
View Article and Find Full Text PDFCancer Cell Int
January 2025
School of Medicine, Kashan University of Medical Sciences, Kashan, Iran.
This narrative review explores the link between breast cancer and night shift work in nurses, focusing on genetic and epigenetic factors. Breast cancer disproportionately affects women globally, and night shift work is increasingly recognized as a potential risk factor. Nurses who work consecutive overnight shifts face elevated risks due to disruptions in their circadian rhythms.
View Article and Find Full Text PDFGenome Biol
January 2025
Institute for Integrative Biology of the Cell (I2BC), Université Paris-Saclay, Centre National de La Recherche Scientifique (CNRS), Commissariat À L'EnergieAtomique (CEA), Gif-Sur-Yvette, 91190, France.
Background: The DNA/H3K9 methylation and Polycomb-group proteins (PcG)-H3K27me3 silencing pathways have long been considered mutually exclusive and specific to transposable elements (TEs) and genes, respectively in mammals, plants, and fungi. However, H3K27me3 can be recruited to many TEs in the absence of DNA/H3K9 methylation machinery and sometimes also co-occur with DNA methylation.
Results: In this study, we show that TEs can also be solely targeted and silenced by H3K27me3 in wild-type Arabidopsis plants.
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