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Updated: Jun 24, 2026

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Generation of a Mouse Spontaneous Autoimmune Thyroiditis Model
Published on: March 17, 2023
Targeting METTL3 Attenuates Thyroid Inflammatory Injury by Restoring Th17/Treg Balance through a YTHDC2-m6A-Dependent
Qingyi Hu1, Huan Liu1, Anwen Ren1
1Department of Breast and Thyroid Surgery, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Advanced Science (Weinheim, Baden-Wurttemberg, Germany)
|June 23, 2026
Summary
Methyltransferase-like 3 (METTL3) drives autoimmune thyroiditis (AIT) by promoting inflammation and thyroid injury. Inhibiting METTL3 alleviates thyroid damage by targeting the KDR/VEGFA signaling pathway.
Area of Science:
- Endocrinology
- Immunology
- Molecular Biology
Background:
- Autoimmune thyroiditis (AIT) involves lymphocytic infiltration and thyroid follicular cell destruction.
- The molecular mechanisms driving persistent thyroid injury in AIT are not fully understood.
Purpose of the Study:
- To investigate the role of methyltransferase-like 3 (METTL3) and N6-methyladenosine (m6A) modification in autoimmune thyroiditis.
- To explore the METTL3-KDR axis as a potential therapeutic target for AIT.
Main Methods:
- Assessed METTL3 expression and m6A levels in thyroid tissues from AIT patients and mice.
- Utilized genetic and pharmacological inhibition of METTL3 in experimental autoimmune thyroiditis (EAT) models.
- Investigated the interaction between METTL3, KDR, VEGFA, and inflammatory pathways.
Main Results:
- METTL3 expression and m6A levels were elevated in AIT thyroid cells and correlated with inflammation.
- METTL3 inhibition reduced inflammation, suppressed KDR/VEGFA signaling, and alleviated thyroid injury.
- ROS promoted METTL3 transcription, while METTL3 stabilized KDR mRNA, creating a positive feedback loop.
Conclusions:
- METTL3 is a key driver of chronic thyroid inflammation in AIT through the METTL3-KDR axis.
- Targeting METTL3 or the KDR/VEGFA pathway offers a promising therapeutic strategy for autoimmune thyroiditis.
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