METTL3 Induces AAA Development and Progression by Modulating N6-Methyladenosine-Dependent Primary miR34a Processing.

ABSTRACT: Identifying effective drugs to delay the progression of aortic aneurysms is a formidable challenge in vascular medicine. Methyltransferase-like 3 (METTL3) plays a key role in catalyzing the formation of N6-methyladenosine (m⁶A), but despite the functional importance of METTL3 and m⁶A in various fundamental biological processes, their roles in abdominal aortic aneurysm (AAA) are unknown. Here, we found that METTL3 knockdown in apolipoprotein E-deficient (ApoE^-/-) mice treated with angiotensin II suppressed the formation of AAAs, while METTL3 overexpression exerted the opposite effects. Similar results were obtained in a calcium chloride (CaCl₂)-induced mouse AAA model. Mechanistically, METTL3-dependent m⁶A methylation promoted primary m

SUBMITTER: Zhong L 

PROVIDER: S-EPMC7347714 | biostudies-literature | 2020 Sep

REPOSITORIES: biostudies-literature