When delivered into mouse hearts following experimental MI, T-cell-derived EVs worsened post-MI cardiac dysfunction via the repression of the miR-142-3p target, adenomatous polyposis coli in cardiac fibroblasts, stimulating up-regulation of WNT-signalling, and pro-fibrotic pathways116 (Figure 4A). This evidence concerns the gene APC and myocardial infarction.