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Updated: Oct 1, 2025
A Method for Measuring RNA N6-methyladenosine Modifications in Cells and Tissues
Published on: December 5, 2016
Role of N6-methyladenosine modification in pathogenesis of ischemic stroke
Hongtao Chang1, Jun Yang1, Qianwen Wang1
1Department of Neurology, The First Affiliated Hospital of China Medical University, Shenyang, Liaoning, China.
Introduction:
N6-Methyladenosine (m6A), the most common and reversible mRNA modification, has attracted considerable attention recently, and accumulating evidence indicates it has an important role in the progression of ischemic stroke (IS).
Areas Covered:
We first reviewed m6A methylation modification enzymes, including m6A methyltransferases (METTL3, METTL14, and WTAP), demethylases (FTO and ALKBH5), m6A-binding proteins (YTH domain containing 1/2 [YTHDC1/2], YTHDF1/2/3, and insulin like growth factor 2 mRNA binding protein 1/2/3 [IGF2BP1/2/3]), and their-related functions. An alteration in the m6A methylation profile of IS has been reported and m6A is differentially expressed in IS. Thus, we then focused on the underlying mechanism of m6A methylation in IS and the involvement of atherosclerosis (AS), cerebral ischemia/reperfusion (IR) injury, inflammation, oxidative stress, and apoptosis. Furthermore, we also elucidated the effect of m6A-associated single-nucleotide polymorphisms (SNPs) on stroke and uncovered new causal variants for IS. The clinical application of m6A targeting drugs is still in its infancy and will be available in the future.
Expert Opinion:
Collectively, the information in the present review is a summary of the latest developments in m6A modification and highlights the mechanisms underlying IS pathogenesis, which may provide novel insights into the mechanisms and therapeutic targets for IS.
Insights
N6-Methyladenosine (m6A) plays a key role in ischemic stroke (IS) progression. This review summarizes m6A
Area of Science:
- Epigenetics and RNA modifications
- Molecular mechanisms of ischemic stroke
Background:
- N6-Methyladenosine (m6A) is the most prevalent and reversible mRNA modification.
- Emerging evidence links m6A modification to the pathogenesis of ischemic stroke (IS).
- Understanding m6A's role is crucial for developing novel IS therapies.
Purpose of the Study:
- To review m6A methylation enzymes and their functions.
- To elucidate the mechanisms of m6A involvement in IS.
- To explore the potential of m6A as a therapeutic target for IS.
Main Methods:
- Comprehensive literature review of m6A modification enzymes (methyltransferases, demethylases, binding proteins).
- Analysis of m6A alterations in IS, including its association with atherosclerosis, IR injury, inflammation, oxidative stress, and apoptosis.
- Investigation of m6A-associated single-nucleotide polymorphisms (SNPs) in IS.
Main Results:
- Detailed overview of m6A methyltransferases (METTL3, METTL14, WTAP), demethylases (FTO, ALKBH5), and m6A-binding proteins (YTHDC1/2, YTHDF1/2/3, IGF2BP1/2/3).
- m6A is differentially expressed in IS, implicating it in key pathological processes.
- Identification of m6A-associated SNPs as potential causal variants for IS.
Conclusions:
- m6A modification is intricately involved in the pathogenesis of ischemic stroke.
- Targeting m6A pathways offers promising therapeutic strategies for IS.
- Further research into m6A-based therapies is warranted for clinical application.
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