Why the study?
Myocardial infarction is a complex, multifactorial pathophysiologic process whose underlying pathogenesis remains unclear.
Multi-omics analysis of a mouse MI model reveals early immune system activation and identifies Nppa, Serpina3n, and Anxa1 as potential circulating biomarkers for myocardial infarction.
As the most severe manifestation of coronary artery disease, myocardial infarction (MI) is a complex and multifactorial pathophysiologic process. However, the pathogenesis that underlies MI remains unclear. Here, we generated a MI mouse model by ligation of the proximal left anterior descending coronary artery. The transcriptome and proteome, at different time points after MI, were detected and analysed. Immune-related pathways, cell cycle-related pathways, and extracellular matrix remodelling-related pathways were significantly increased after MI. Not only innate immune cells but also adaptive immune cells participated in the early stage of MI. Proteins that functioned in blood agglutination, fibrinolysis, secretion, and immunity were significantly changed after MI. Nppa, Serpina3n, and Anxa1, three secreted proteins that can easily be detected in blood, were significantly changed after MI. Our discoveries not only reveal the molecular and cellular changes in MI but also identify potential candidate biomarkers of MI for clinical diagnosis or treatment.
No takes yet. Share an insight, caveat, or question.
Li et al. (2019) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: