Myocardial infarction is accompanied by abnormal glucose and lipid metabolism in most patients, but its mechanism remains unclear. In this special issue on glucose and lipid metabolism, researchers report that a new cardiomyocyte pyroptosis-associated lncRNA (CPAL) is an important regulatory molecule of myocardial glucose and lipid metabolism dysfunction, and that targeted inhibition of the CPAL-mediated NFκb–caspase-1 signaling pathway improves glucose and lipid metabolism dysfunction and inhibits cardiomyocyte pyroptosis after myocardial infarction. This finding may promote the research and development of drugs for the treatment of myocardial inflammation and disorder of glucose and lipid metabolism after myocardial infarction.