Methyltransferase like 3 promotes thyroid folliculogenesis <i>via</i> coordinating cell differentiation and polarization.

ABSTRACT:

Background and objectives

Congenital hypothyroidism (CH) is the most common neonatal endocrine disorder with largely elusive underlying mechanisms, although thyroid dysformation has been deemed as the most frequent cause. Methyltransferase like 3 (METTL3) serves as a pivotal writer for N⁶-methyladenosine (N6-methyladenosine, m⁶A) required for various organ development, but little is known about the significance of METTL3 and m⁶A modification in thyroid formation, in CH either. In this study, we aimed to clarify the new regulatory role of METTL3 in the occurrence and development of CH, and to provide new theoretical support and treatment ideas for the clinical treatment of CH.

Methods

Thyrocyte-specific Mettl3 knockout mouse model was c

SUBMITTER: Jiang R 

PROVIDER: S-EPMC12916267 | biostudies-literature | 2026 Feb

REPOSITORIES: biostudies-literature