METTL3 mediates atheroprone flow-induced glycolysis in endothelial cells

• 成果类型: Article
• 署名作者: Zhao, Guo - Jun; Han, So Yun; Li, Yajuan; Yuan, Dongqiang; Qin, Shuo; Li, Yuhan; Jang, Hongje; Chen, Li - Jing; Wei, Tong - You Wade; He, Ming; Li, Yi - Shun; Chen, Zhen Bouman; Shi, Lingyan; Chien, Shu; Shyy, John Y- J.
• 署名单位: Zhengzhou University; University of California System; University of California San Diego; University of California System; University of California San Diego; City of Hope; Beckman Research Institute of City of Hope
• 刊物名称: PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
• ISSN/ISSBN: 0027-14541
• DOI: 10.1073/pnas.2424796122
• 发表日期: 2025-05-13
• 关键词: metabolism; HEALTH

摘要

Atheroprone flow-increased glycolysis in vascular endothelial cells (ECs) is pivotal in is a major m6A methyltransferase for RNA N6- mehtyladenosine (m6A) modifications to regulate epitranscriptome and cellular functions. With the atheroprone flow upreguin atheroprone flow-induced glycolysis in ECs in vitro and in vivo. Compared to pulflow) increases METTL3 expression to enhance the m6A modifications of mRNAs encoding HK1, PFKFB3, and GCKR, which are rate- limiting enzymes of glycolysis. while decreasing GCKR, resulting in elevated EC glycolysis, as revealed by seahorse anotransduction with metabolic reprogramming under atherogenic conditions.