Abstract
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.
Highlights
Myocardial infarction (MI), the most severe manifestation of coronary artery disease, causes more than 6.4 million deaths in the US, Europe, and Northern Asia and more than a third of the deaths in developed nations each year[1,2]
Myocardial fibrosis is one of the main events after MI, so we evaluated the model by detecting the degree of myocardial fibrosis[8,12]
Masson staining displayed the fibres in the myocardium as blue, and the staining depth reflected the degree of fibrosis
Summary
Myocardial infarction (MI), the most severe manifestation of coronary artery disease, causes more than 6.4 million deaths in the US, Europe, and Northern Asia and more than a third of the deaths in developed nations each year[1,2]. Exploration of integrated cellular and molecular characteristics of MI may help to deepen the understanding of myocardial dysfunction during MI, leading to the establishment of personalised treatment and prevention strategies and improvements in patients’ clinical outcomes[4]. MI is a complex process with different components, including cell hypoxia, apoptosis, migration, fibrosis, and immune cell infiltration. Zhu et al suggested vascular endothelial cell migration and apoptosis that was induced by iNOS play a crucial role in MI5. The roles of immune cells in this process have not been identified clearly
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