Edil3, also known as EDIL3/Del-1, is a secreted protein containing epidermal growth factor-like repeats and discoidin I-like domains. It plays crucial roles in multiple biological processes such as embryonic development, inflammatory regulation, and angiogenesis, and is involved in pathways like integrin-mediated cell adhesion [2,3,4,5]. Genetic models, especially knockout mice, have been instrumental in studying its functions.

In cardiac remodelling after myocardial infarction (MI), Edil3-/-mice showed improved post-MI adverse remodelling with lower mortality, better cardiac function, and less fibrosis. EDIL3 deficiency enhanced neutrophil recruitment and a specific pro-inflammatory macrophage polarization through neutrophil extracellular traps (NETs), revealing its role in NET-primed macrophage polarization during MI [1]. In thoracic aortic dissection, global edil3 knockout mice had exacerbated disease with more apoptotic vascular smooth muscle cells (VSMCs) accumulating in the aorta, as edil3-deficient phagocytes were less efficient in internalizing and degrading apoptotic VSMCs [2]. In psoriatic arthritis, Edil3 knockout mice had a more severe phenotype, and recombinant EDIL3 protein injection alleviated the disease by regulating the activation of monocyte-derived DCs and Th17 cells and attenuating intracellular glycolysis in MoDCs [6].

In conclusion, Edil3 is essential in maintaining normal physiological functions and its dysregulation is associated with various diseases. Studies using Edil3 knockout mouse models have significantly contributed to understanding its roles in cardiac remodelling after MI, aortic dissection, and psoriatic arthritis, providing potential therapeutic targets for these diseases.