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Key m6A regulators mediated methylation modification pattern and immune infiltration characterization in hepatic

Yixi Zhang1, Can Qi2, Yiwen Guo3

  • 1Department of General Surgery, Beijing Friendship Hospital, Capital Medical University, NO. 95 Yongan Road, Beijing, 100051, China.

BMC Medical Genomics
|December 4, 2023
PubMed
Abstract

Insights

N6-methyladenosine (m6A) mRNA regulators impact hepatic ischemia-reperfusion injury (IRI). This study identified key m6A regulators and their correlation with immune cells, offering potential therapeutic targets for hepatic IRI.

Area of Science:

  • Epigenetics
  • Molecular Biology
  • Immunology

Background:

  • N6-methyladenosine (m6A) mRNA modification is crucial in biological processes.
  • Its role in hepatic ischemia-reperfusion injury (IRI) remains unexplored.
  • This study investigates m6A regulators in hepatic IRI.

Purpose of the Study:

  • To explore the expression patterns of m6A regulators in hepatic IRI.
  • To identify potential functions of m6A regulators in hepatic IRI.
  • To establish predictive models for hepatic IRI risk.

Main Methods:

  • Analysis of gene expression data (GSE23649) of m6A regulators in human liver tissues.
  • Screening of candidate m6A regulators using random forest (RF) model.
  • Validation in a mouse hepatic IRI model using qRT-PCR and immune cell infiltration analysis.

Main Results:

  • Differential expression of m6A regulators (e.g., WTAP, CBLL1, FTO, METTL3) observed in hepatic IRI.
  • Eight m6A regulators identified for hepatic IRI risk prediction via RF model.
  • Correlation between m6A regulators and infiltration of various immune cells (e.g., T cells, myeloid-derived suppressor cells, macrophages).

Conclusions:

  • m6A regulators significantly influence hepatic IRI.
  • Identified m6A patterns may offer novel therapeutic targets for hepatic IRI.
  • Further research into m6A modification could lead to new treatment strategies for hepatic IRI.
Keywords:
Hepatic ischemia-reperfusion injuryMETTL3YTHDC1m6A methylation regulators

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