Progress in epigenetic regulation of milk synthesis, with particular emphasis on mRNA regulation and DNA methylation.
Cell Cycle
; 22(14-16): 1675-1693, 2023.
Article
em En
| MEDLINE
| ID: mdl-37409592
ABSTRACT
Inadequate milk secretion and a lack of nutrients in humans and mammals are serious problems. It is of great significance to clarify the mechanisms of milk synthesis and treatment methods. Epigenetic modification, represented by RNA methylation, is an important way of gene expression regulation that profoundly affects human gene expression and participates in various physiological and pathological mechanisms. Epigenetic disorders also have an important impact on the production and secretion of milk. This review systematically summarized the research results of epigenetics in the process of lactation in PubMed, Web of Science, NSTL, and other databases and reviewed the effects of epigenetics on human and mammalian lactation, including miRNAs, circRNAs, lncRNAs, DNA methylations, and RNA methylations. The abnormal expression of miRNAs was closely related to the synthesis and secretion of milk fat, milk protein, and other nutrients in the milk of cattle, sheep, and other mammals. MiRNAs are also involved in the synthesis of human milk and the secretion of nutrients. CircRNAs and lncRNAs mainly target miRNAs and regulate the synthesis of nutrients in milk by ceRNA mechanisms. The abnormal expression of DNA and RNA methylation also has an important impact on milk synthesis. Epigenetic modification has the potential to regulate the milk synthesis of breast epithelial cells. Analyzing the mechanisms of human and mammalian milk secretion deficiency and nutrient deficiency from the perspective of epigenetics will provide a new perspective for the treatment of postpartum milk deficiency in pregnant women and mammalian milk secretion deficiency.
Palavras-chave
Texto completo:
1
Base de dados:
MEDLINE
Assunto principal:
MicroRNAs
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RNA Longo não Codificante
Limite:
Animals
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Female
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Humans
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Pregnancy
Idioma:
En
Ano de publicação:
2023
Tipo de documento:
Article