Exploring the potential mechanisms of m6A modification in septic acute respiratory distress syndrome: a

Shaoyang Zhang1, Qinghui Fu2, Zhipeng Xu3

  • 1The Department of Emergency, The First Affiliated Hospital, Zhejiang University School of Medicine, Qingchun Street 79th, Hangzhou, Zhejiang Province, 310003, China.

Hereditas
|June 23, 2025
PubMed
Abstract

Insights

WTAP promotes acute respiratory distress syndrome (ARDS) by altering N6-methyladenosine (m6A) methylation and increasing immune cell infiltration. This study highlights WTAP as a key regulator in ARDS progression.

Area of Science:

  • Molecular Biology
  • Immunology
  • Genomics

Background:

  • Acute respiratory distress syndrome (ARDS) is a major cause of ICU mortality.
  • The role of N6-methyladenosine (m6A) mRNA modification in ARDS, especially at the single-cell level, is not well understood.

Purpose of the Study:

  • To investigate the role of m6A regulators in the ARDS microenvironment.
  • To identify potential therapeutic targets for ARDS.

Main Methods:

  • Single-cell and bulk RNA-sequencing data analysis.
  • Bioinformatics approaches including WGCNA.
  • Experimental validation in lung tissues and functional assays.

Main Results:

  • WTAP, HNRNPA2B1, and HNRNPC were highly expressed in the ARDS microenvironment.
  • WTAP expression varied across sepsis patient subgroups.
  • WTAP was associated with five hub genes and promoted ARDS progression.

Conclusions:

  • WTAP promotes ARDS onset and progression.
  • WTAP regulates m6A methylation and immune cell infiltration in ARDS.
  • WTAP is a potential therapeutic target for ARDS.