Energy Metabolism Dysregulation in Myocardial Infarction: An Integrative Analysis of Ischemic Cardiomyopathy.

BACKGROUND: Myocardial metabolism is closely related to functional changes after myocardial infarction (MI). OBJECTIVE: This study aimed to present an integrative examination of human ischemic cardiomyopathy. METHODS: We used both GSE121893 single-cell suspension sequencing and GSE19303 transcription microarray data sets from the GEO database, along with a murine MI model for full-spectrum metabolite detection. Through a systematic investigation that involved differential metabolite identification and functional enrichment analysis, we shed light on the pivotal role of energy metabolism dysregulation in the progression of MI. RESULTS: Our findings revealed an association between the core regulatory genes CDKN1A, FOS, ITGB4, and MAP2K1 and the underlying pathophysiology of the disease. These genes are identified as critical elements in the complex landscape of myocardial ischemic disorder, highlighting novel insights into therapeutic targets and the intricate biological mechanisms involved. CONCLUSION: This analysis provides a framework for future research on the metabolic alterations associated with MI.

SGLT2 inhibitor improves the prognosis of patients with coronary heart disease and prevents in-stent restenosis.

Coronary heart disease is a narrowing or obstruction of the vascular cavity caused by atherosclerosis of the coronary arteries, which leads to myocardial ischemia and hypoxia. At present, percutaneous coronary intervention (PCI) is an effective treatment for coronary atherosclerotic heart disease. Restenosis is the main limiting factor of the long-term success of PCI, and it is also a difficult problem in the field of intervention. Sodium-glucose cotransporter 2 (SGLT2) inhibitor is a new oral glucose-lowering agent used in the treatment of diabetes in recent years. Recent studies have shown that SGLT2 inhibitors can effectively improve the prognosis of patients after PCI and reduce the occurrence of restenosis. This review provides an overview of the clinical studies and mechanisms of SGLT2 inhibitors in the prevention of restenosis, providing a new option for improving the clinical prognosis of patients after PCI.