Abstract
Aberrant sphingolipid metabolism contributes to cardiac pathophysiology. Emerging evidence found that an increased level of ceramide during the inflammatory phase of post-myocardial infarction (MI) served as a biomarker and was associated with cardiac dysfunction. However, the alternation of the sphingolipid profile during the reparative phase after MI is still not fully understood. Using a mouse model of the left anterior descending ligation that leads to MI, we performed metabolomics studies to assess the alternations of both plasma and myocardial sphingolipid profiles during the reparative phase post-MI. A total number of 193 sphingolipid metabolites were detected. Myocardial sphingolipids but not plasma sphingolipids showed marked change after MI injury. Ceramide-1-phosphates, which were accumulated after MI, contributed highly to the difference in sphingolipid profiles between groups. Consistently, the expression of ceramide kinase, which phosphorylates ceramides to generate ceramide-1-phosphates, was upregulated in heart tissue after MI injury. Our findings revealed the altering sphingolipid metabolism during the reparative phase post-MI and highlighted the potential role of ceramide kinase/ceramide-1-phosphate in ischemic heart disease.
Highlights
Cardiovascular diseases were the most common underlying cause of death in the world, accounting for an estimated 31.5% of all global deaths (Benjamin et al, 2019)
Cardiac inflammation and resolution are critical to the severity of cardiac dysfunction post-myocardial infarction (MI) and abnormal lipid metabolism contributes to myocardial injury and remodeling
We observed the alternation of the sphingolipid profile during the reparative phage after MI injury
Summary
Cardiovascular diseases were the most common underlying cause of death in the world, accounting for an estimated 31.5% of all global deaths (Benjamin et al, 2019). Heart failure (HF) after myocardial infarction (MI) is the major driver of late morbidity, mortality, and healthcare cost (Cahill and Kharbanda, 2017). Since both the incidence and prevalence of post-MI leading to HF have continually climbed (Benjamin et al, 2019), it is important to identify treatable conditions potentially contributive to HF progression. Increased attention has been focused on perturbed sphingolipid metabolism associated with cardiovascular diseases (Laaksonen et al, 2016; Parveen et al, 2019), highlighting the importance to study the alteration of sphingolipid profile in a certain condition and the underlying mechanism
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