Related Experiment Video
Updated: Jan 9, 2026

14:40
Exploring m6A and m5C Epitranscriptomes upon Viral Infection: an Example with HIV
Published on: March 5, 2022
3.7K
Research advances in m6A methylation and sepsis
Lifan Zhang1,2, Wenjuan Chen1,2, Yafeng Liu1,2
1Department of Infectious Diseases, The First Affiliated Hospital, College of Clinical Medicine, Henan University of Science and Technology, Luoyang, Henan, China.
Frontiers in Cell and Developmental Biology
|December 4, 2025
Summary
Sepsis causes organ damage through inflammation. N6-methyladenosine (m6A) RNA modification plays a key role in this process and may be a therapeutic target for sepsis.
Area of Science:
- Epigenetics
- Molecular Biology
- Immunology
Background:
- Sepsis is a life-threatening organ dysfunction caused by a dysregulated host response to infection.
- N6-methyladenosine (m6A) is the most abundant RNA modification in eukaryotes, regulating gene expression.
- m6A modification is dynamically regulated by writers, erasers, and readers, influencing various biological processes.
Purpose of the Study:
- To review the mechanistic insights into the role of m6A in sepsis pathogenesis.
- To explore the involvement of m6A dysregulation in sepsis-induced multi-organ damage.
- To evaluate the therapeutic potential of targeting m6A in sepsis.
Main Methods:
- Literature review synthesizing current research on m6A and sepsis.
- Analysis of mechanisms by which m6A influences inflammatory responses.
- Evaluation of evidence linking m6A to organ-specific injury in sepsis models.
Main Results:
- m6A dysregulation is implicated in cardiovascular dysfunction, acute lung injury, and acute kidney injury during sepsis.
- m6A governs inflammatory cascades and organ injury pathways.
- Specific m6A regulators (writers, erasers, readers) are involved in sepsis progression.
Conclusions:
- m6A is a critical regulator in sepsis pathogenesis and multi-organ dysfunction.
- Targeting m6A pathways offers potential therapeutic strategies for sepsis.
- Further research is needed to develop translational frameworks for m6A-based sepsis therapies.

