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Mitoepigenetics and gliomas: epigenetic alterations to mitochondrial DNA and nuclear DNA alter mtDNA expression and contribute to glioma pathogenicity. [Review]

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Citation: Frontiers in neurology [electronic resource].. 14:1154753, 2023.PMID: 37332990Department: MedStar Georgetown University Hospital/MedStar Washington Hospital Center | Neurosurgery ResidencyForm of publication: Journal ArticleMedline article type(s): Journal Article | ReviewSubject headings: Year: 2023 ISSN:

1664-2295

Name of journal: Frontiers in neurologyAbstract: 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 noncoding RNAs [RNA mitochondrial RNA processing (RMRP)] have all been identified as contributing to glioma pathogenicity. Developing new interventions interfering with these pathways may improve glioma therapy. Copyright © 2023 Grady, Walsh and Heiss.All authors: Grady CI, Heiss JD, Walsh LMFiscal year: FY2023 Digital Object Identifier:

https://dx.doi.org/10.3389/fneur.2023.1154753

Date added to catalog: 2023-07-21

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Holdings
Item type	Current library	Collection	Call number	Status	Date due	Barcode
Journal Article	MedStar Authors Catalog	Article	37332990	Available		37332990

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 noncoding RNAs [RNA mitochondrial RNA processing (RMRP)] have all been identified as contributing to glioma pathogenicity. Developing new interventions interfering with these pathways may improve glioma therapy. Copyright © 2023 Grady, Walsh and Heiss.

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