Expression profiling by high throughput sequencing

Fibrotic scarring is tightly linked to the development of heart failure in patients post-myocardial infarction (MI). ACKR4 is an atypical chemokine receptor, which can eliminate homeostatic chemokines, such as CCL21 which is independently associated with mortality in patients with ischemic heart failure. However, the role of ACKR4 in the heart during MI is not completely understood. We show here that ACKR4 is upregulated in the heart after MI in mice. Knockout of ACKR4 ameliorated heart functional impairment post-MI. In this dataset, we include the expression data obtained from cardiac tissues of WT and ACKR4-KO mice at day 14 post-MI. It revealed that ACKR4 deletion resulted in strongly downregulated expression of genes related to extracellular matrix, chemotaxis and cytokine activity.