Therefore, based on the experimental results presented in Sects. "MTH reduced myocardial infarction area and improved hemodynamic performance after ischemia–reperfusion injury in rats" to "MTH upregulates the level of O-GlcNAcylation-modified COX10 and promotes its transfer to mitochondria", we propose the following hypothesis: MTH improves mitochondrial function by regulating the O-GlcNAcylation level of COX10 and promoting its entry into mitochondria, thereby exerting its cardioprotective effects in myocardial ischemia–reperfusion injury. Here, COX10 is linked to myocardial ischemia.