Given the conspicuous differences in HV and IS patient plasma endostatin levels and the role of this anti-angiogenic factor in EPC functionality and post-stroke angiogenesis [47, 48], this study specifically assessed the impact of OEC-CM on endostatin levels in HBMEC and OEC subjected to TNF-α and significantly inhibited TNF-α-mediated elevations observed in both cell types (Supplementary Fig. 9). This evidence concerns the gene COL18A1 and stroke disorder.