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Updated: Jun 15, 2025
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Published on: March 15, 2024
The regulatory mechanisms of N6-methyladenosine modification in ferroptosis and its implications in disease
Xiao Tao1, Ningning Kang2, Zongqin Zheng3
1Department of Clinical Medicine, The First School of Clinical Medicine, Anhui Medical University, Hefei, Anhui 230032, PR China.
Heading Aims:
Based on the current knowledge of the molecular mechanisms by which m6A influences ferroptosis, our objective is to underscore the intricate and interdependent relationships between m6A and the principal regulatory pathways of ferroptosis, as well as other molecules, emphasizing its relevance to diseases associated with this cell death mode.
Materials And Methods:
We conducted a literature search using the keywords "m6A and ferroptosis" across PubMed, Web of Science, and Medline. The search was limited to English-language publications from 2017 to 2024. Retrieved articles were managed using Endnote software. Two authors independently screened the search results and reviewed the full texts of selected articles.
Key Findings:
Abnormal m6A levels are often identified as critical regulators of ferroptosis. Specifically, "writers", "readers" and "erasers" that dynamically modulate m6A function regulate various pathways in ferroptosis including iron metabolism, lipid metabolism and antioxidant system. Additionally, we provide an overview of the role of m6A-mediated ferroptosis in multiple diseases and summarize the potential applications of m6A-mediated ferroptosis, including its use as a therapeutic target for diseases and as diagnostic as well as prognostic biomarkers.
Significance:
N6-methyladenosine (m6A) modification, a prevalent RNA modification in eukaryotic cells, is crucial in regulating various aspects of RNA metabolism. Notably, accumulating evidence has implicated m6A modification in ferroptosis, a form of iron-dependent cell death characterized by elevated iron levels and lipid peroxide accumulation. Overall, this review sheds light on the potential diagnostic and therapeutic applications of m6A regulators in addressing conditions associated with ferroptosis.
Insights
N6-methyladenosine (m6A) regulates ferroptosis, a cell death pathway. This review explores m6A
Area of Science:
- Molecular Biology
- Cell Death Mechanisms
- RNA Modifications
Background:
- N6-methyladenosine (m6A) is a prevalent RNA modification influencing gene expression.
- Ferroptosis is an iron-dependent form of programmed cell death characterized by lipid peroxidation.
- Dysregulation of m6A is increasingly linked to various pathological conditions.
Purpose of the Study:
- To elucidate the molecular mechanisms connecting m6A modification and ferroptosis.
- To highlight the interplay between m6A regulators and ferroptosis pathways.
- To emphasize the relevance of m6A-mediated ferroptosis in disease.
Main Methods:
- Comprehensive literature search on "m6A and ferroptosis" in PubMed, Web of Science, and Medline (2017-2024).
- Systematic screening and full-text review of retrieved English-language articles.
- Synthesis of findings regarding m6A's role in ferroptosis regulation and disease.
Main Results:
- Abnormal m6A levels are critical regulators of ferroptosis.
- "Writers", "readers", and "erasers" of m6A dynamically control ferroptosis pathways, including iron metabolism, lipid metabolism, and antioxidant systems.
- m6A-mediated ferroptosis plays a role in multiple diseases, offering potential as therapeutic targets and diagnostic/prognostic biomarkers.
Conclusions:
- m6A modification is integral to regulating RNA metabolism and is implicated in ferroptosis.
- Understanding m6A's role in ferroptosis provides insights into iron-dependent cell death.
- m6A regulators hold significant potential for diagnosing and treating ferroptosis-associated diseases.
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