能量供应不足所致的心肌细胞凋亡是导致AMI后病情进一步恶化的重要因素，而糖酵解途径是AMI后为心肌供能的最主要途径，PFK1作为糖酵解途径的关键酶，发挥了重要作用。前期研究表明，AMI后小鼠心肌产能下降，并伴有O-GlcNAc糖基化水平升高，其中包括PFK1的O-GlcNAc糖基化水平升高。据此提出假设：AMI后，PFK1通过O-GlcNAc糖基化调节能量供应，进而影响心肌细胞凋亡。本项目拟通过体外实验验证O-GlcNAc糖基化对PFK1活性的影响，确定其糖基化位点；通过在体/离体模型观察PFK1的O-GlcNAc糖基化对糖酵解途径、细胞产能、细胞凋亡、心功能的影响，确定PFK1的O-GlcNAc糖基化对能量供应不足所致的心肌细胞凋亡的作用机制，并尝试调节AMI后PFK1的糖基化水平，影响心肌细胞的能量供应，从而实现保护心肌细胞的目的。为进一步探索AMI病情发展提供新理论和药物治疗的靶点。

Apoptosis due to insufficient energy supply is the main cause in the progression of acute myocardial infarction. Glycolysis is the main metabolic pathway for providing energy during ischemia. As an important regulatory enzyme in glycolysis, PFK1 plays an essential rule in metabolic pathway. Previous research indicated that, the ATP production of mice myocardial tissue decreased, and the whole level of O-GlcNAcylation in mice myocardial tissue increased, as well as PFK1 O-GlcNAcylation during ischemia. The hypothesis of this study is: the activity of PFK1 during ischemia is regulated by O-GlcNAcylation, which can directly induce the glycolysis pathway, ATP production and apoptosis. In this study, we plan to research the O-GlcNAcylated site of PFK1 and the changes of enzyme activity. Furthermore, we will research the mechanism of PFK1 O-GlcNAcylation on energy metabolism and apoptosis in AMI. Our study will provide fundamental basis and AD-targeted drugs for further exploring of AMI progression.