Aubert Gregory, Barefield David Y, Demonbreun Alexis R, Ramratnam Mohun, Fallon Katherine S, Warner James L, Rossi Ann E, Hadhazy Michele, Makielski Jonathan C, McNally Elizabeth M
Center for Genetic Medicine, Northwestern University Feinberg School of Medicine, Chicago Illinois.
Division of Cardiology, Department of Medicine, University of Wisconsin-Madison, Madison, Wisconsin.
JACC Basic Transl Sci. 2019 Apr 29;4(2):251-268. doi: 10.1016/j.jacbts.2018.11.012. eCollection 2019 Apr.
The adult myocardium relies on oxidative metabolism. In ischemic myocardium, such as the embryonic heart, glycolysis contributes more prominently as a fuel source. The sulfonylurea receptor 2 (SUR2) was previously implicated in the normal myocardial transition from glycolytic to oxidative metabolism that occurs during adaptation to postnatal life. This receptor was now selectively deleted in adult mouse myocardium resulting in protection from ischemia reperfusion injury. SUR2-deleted cardiomyocytes had enhanced glucose uptake, and SUR2 forms a complex with the major glucose transporter. These data identify the SUR2 receptor as a target to shift cardiac metabolism to protect against myocardial injury.
成年心肌依赖氧化代谢。在缺血心肌中,如胚胎心脏,糖酵解作为一种燃料来源发挥着更突出的作用。磺脲类受体2(SUR2)先前被认为与心肌在适应出生后生活过程中从糖酵解代谢向氧化代谢的正常转变有关。现在在成年小鼠心肌中选择性删除该受体可使其免受缺血再灌注损伤。删除SUR2的心肌细胞葡萄糖摄取增强,且SUR2与主要的葡萄糖转运体形成复合物。这些数据表明SUR2受体是改变心脏代谢以预防心肌损伤的一个靶点。