Network analysis of these enriched genes (Fig. 5C) shows the complex interplay between the various biological processes and the bridging roles played by Abi3bp, Adam8, Ccl7, Ccl8, Comp, Il1b, Mfge8, Sfrp2, and Trem2. An eminent mediator of this extracellular remodelling can be attributed to the increased Thbs4 expression in the heart, which has been shown to promote fibrosis and extracellular matrix disassembly following ischemia [35]. The gene discussed is CCL8; the disease is ischemia.