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RNA m6A methylation regulators in sepsis.
Zhu, Lin; Zhang, Hairong; Zhang, Xiaoyu; Xia, Lei.
Afiliação
  • Zhu L; School of Chinese Medicine, Shandong University of Traditional Chinese Medicine, Jinan, People's Republic of China.
  • Zhang H; Department of Obstetrics and Gynecology, Shandong Provincial Third Hospital, Jinan, 250031, People's Republic of China. sdzhhr7211@163.com.
  • Zhang X; School of Chinese Medicine, Shandong University of Traditional Chinese Medicine, Jinan, People's Republic of China.
  • Xia L; Department of Pathology, Shandong University of Traditional Chinese Medicine, Jinan, 250355, People's Republic of China. pathology001@sina.com.
Mol Cell Biochem ; 2023 Sep 02.
Article em En | MEDLINE | ID: mdl-37659034
ABSTRACT
N6-methyladenosine (m6A) modification is a class of epitope modifications that has received significant attention in recent years, particularly in relation to its role in various diseases, including sepsis. Epigenetic research has increasingly focused on m6A modifications, which is influenced by the dynamic regulation of three protein types ?Writers" (such as METTL3/METTL14/WTAP)-responsible for m6A modification; ?Erasers" (FTO and ALKBH5)-involved in m6A de-modification; and ?Readers" (YTHDC1/2, YTHDF1/2/3)-responsible for m6A recognition. Sepsis, a severe and fatal infectious disease, has garnered attention regarding the crucial effect of m6A modifications on its development. In this review, we attempted to summarize the recent studies on the involvement of m6A and its regulators in sepsis, as well as the significance of m6A modifications and their regulators in the development of novel drugs and clinical treatment. The potential value of m6A modifications and modulators in the diagnosis, treatment, and prognosis of sepsis has also been discussed.
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Texto completo: 1 Base de dados: MEDLINE Idioma: En Revista: Mol Cell Biochem Ano de publicação: 2023 Tipo de documento: Article

Texto completo: 1 Base de dados: MEDLINE Idioma: En Revista: Mol Cell Biochem Ano de publicação: 2023 Tipo de documento: Article