Flavin Containing Monooxygenase 2 Prevents Cardiac Fibrosis via CYP2J3-SMURF2 Axis.
Cheng NiYongjian ChenYin-Chuan XuJing ZhaoQingju LiChangchen XiaoYan WuJingyi WangYingchao WangZhiwei ZhongLing ZhangRongrong WuQingnian LiuXianpeng WuChangle KeWei ZhuJinghai ChenJijun HuangYibin WangWangxing HuXinyang HuPublished in: Circulation research (2022)
Loss of FMO2 is a conserved molecular signature in postinjury hearts. FMO2 possesses a previously uncharacterized enzyme-independent antifibrosis activity via the CYP2J3-SMURF2 axis. Restoring FMO2 expression exerts potent ameliorative effect against fibrotic remodeling in postinjury hearts from rodents to nonhuman primates. Therefore, FMO2 is a potential therapeutic target for treating cardiac fibrosis following injury.